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Inflammatory responses in small vessels play an important role in the development of cardiovascular diseases, including hypertension, stroke, and small vessel disease. This involves various complex molecular processes including oxidative stress, inflammasome activation, immune-mediated responses, and protein misfolding, which together contribute to microvascular damage. In addition, epigenetic factors, including DNA methylation, histone modifications, and microRNAs influence vascular inflammation and injury. These phenomena may be acquired during the aging process or due to environmental factors. Activation of proinflammatory signaling pathways and molecular events induce low-grade and chronic inflammation with consequent cardiovascular damage. Identifying mechanism-specific targets might provide opportunities in the development of novel therapeutic approaches. Monoclonal antibodies targeting inflammatory cytokines and epigenetic drugs, show promise in reducing microvascular inflammation and associated cardiovascular diseases. In this article, we provide a comprehensive discussion of the complex mechanisms underlying microvascular inflammation and offer insights into innovative therapeutic strategies that may ameliorate vascular injury in cardiovascular disease., Competing Interests: Disclosures None.

Damage-associated molecular patterns (DAMPs) are endogenous molecules that are released from host cells as a result of cell death or damage. The release of DAMPs in tissues is associated with loss of tissue homeostasis. Sensing of DAMPs by innate immune receptors triggers inflammation, which can be beneficial in initiating the processes that restore tissue homeostasis but can also drive inflammatory diseases. In recent years, the sensing of intracellular DAMPs has received extensive attention in the field of sterile inflammation. However, emerging studies have shown that DAMPs that originate from neighbouring cells, and even from distal tissues or organs, also mediate sterile inflammatory responses. This multi-level sensing of DAMPs is crucial for intercellular, trans-tissue and trans-organ communication. Here, we summarize how DAMP-sensing receptors detect DAMPs from intracellular, intercellular or distal tissue and organ sources to mediate sterile inflammation. We also discuss the possibility of targeting DAMPs or their corresponding receptors to treat inflammatory diseases., (© 2024. Springer Nature Limited.)

Persistent and unresolved inflammation is a common underlying factor observed in several and seemingly unrelated human diseases, including cardiovascular and neurodegenerative diseases. Particularly, in atopic conditions, acute inflammatory responses such as those triggered by insect venom, food or drug allergies possess also a life-threatening potential. However, respiratory allergies predominantly exhibit late immune responses associated with chronic inflammation, that can eventually progress into a severe phenotype displaying similar features as those observed in other chronic inflammatory diseases, as is the case of uncontrolled severe asthma. This review aims to explore the different facets and systems involved in chronic allergic inflammation, including processes such as tissue remodelling and immune cell dysregulation, as well as genetic, metabolic and microbiota alterations, which are common to other inflammatory conditions. Our goal here was to deepen on the understanding of an entangled disease as is chronic allergic inflammation and expose potential avenues for the development of better diagnostic and intervention strategies., (© 2024 The Author(s). Clinical & Experimental Allergy published by John Wiley & Sons Ltd.)

Tissue inflammation is a hallmark of tumour microenvironments. In the bone marrow, tumour-associated inflammation impacts normal niches for haematopoietic progenitor cells and mature immune cells and supports the outgrowth and survival of malignant cells residing in these niche compartments. This Review provides an overview of our current understanding of inflammatory changes in the bone marrow microenvironment of myeloid and lymphoid malignancies, using acute myeloid leukaemia and multiple myeloma as examples and highlights unique and shared features of inflammation in niches for progenitor cells and plasma cells. Importantly, inflammation exerts profoundly different effects on normal bone marrow niches in these malignancies, and we provide context for possible drivers of these divergent effects. We explore the role of tumour cells in inflammatory changes, as well as the role of cellular constituents of normal bone marrow niches, including myeloid cells and stromal cells. Integrating knowledge of disease-specific dynamics of malignancy-associated bone marrow inflammation will provide a necessary framework for future targeting of these processes to improve patient outcome., (© 2024. Springer Nature Limited.)

The European Forum for Research and Education in Allergy and Airways diseases (EUFOREA) organized its bi-annual forum EUFOREUM in Berlin in November 2023. The aim of EUFOREUM 2023 was to highlight pediatric action plans for prevention and optimizing care for type 2 inflammatory conditions starting in childhood, with a focus on early-stage diagnosis, ensuring neither under- nor overdiagnosis, optimal care, and suggestions for improvement of care. EUFOREA is an international not-for-profit organization forming an alliance of all stakeholders dedicated to reducing the prevalence and burden of chronic respiratory diseases through the implementation of optimal patient care via educational, research, and advocacy activities. The inclusive and multidisciplinary approach of EUFOREA was reflected in the keynote lectures and faculty of the virtual EUFOREUM 2023 (www.euforea.eu/euforeum) coming from the pediatric, allergology, pulmonology, ENT, dermatology, primary health care fields and patients around the central theme of type 2 inflammation. As most type 2 inflammatory conditions may start in childhood or adolescence, and most children have type 2 inflammation when suffering from a respiratory or skin disease, the moment has come to raise the bar of ambitions of care, including prevention, remission and disease modification at an early stage. The current report provides a comprehensive overview of key statements by the faculty of the EUFOREUM 2023 and the ambitions of EUFOREA allowing all stakeholders in the respiratory field to be updated and ready to join forces in Europe and beyond., (© 2024 The Author(s). Pediatric Allergy and Immunology published by European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd.)

Hypertension is a global health problem, with >1.3 billion individuals with high blood pressure worldwide. In this Review, we present an inflammatory paradigm for hypertension, emphasizing the crucial roles of immune cells, cytokines and chemokines in disease initiation and progression. T cells, monocytes, macrophages, dendritic cells, B cells and natural killer cells are all implicated in hypertension. Neoantigens, the NLRP3 inflammasome and increased sympathetic outflow, as well as cytokines (including IL-6, IL-7, IL-15, IL-18 and IL-21) and a high-salt environment, can contribute to immune activation in hypertension. The activated immune cells migrate to target organs such as arteries (especially the perivascular fat and adventitia), kidneys, the heart and the brain, where they release effector cytokines that elevate blood pressure and cause vascular remodelling, renal damage, cardiac hypertrophy, cognitive impairment and dementia. IL-17 secreted by CD4 + T helper 17 cells and γδ T cells, and interferon-γ and tumour necrosis factor secreted by immunosenescent CD8 + T cells, exert crucial effector roles in hypertension, whereas IL-10 and regulatory T cells are protective. Effector mediators impair nitric oxide bioavailability, leading to endothelial dysfunction and increased vascular contractility. Inflammatory effector mediators also alter renal sodium and water balance and promote renal fibrosis. These mechanisms link hypertension with obesity, autoimmunity, periodontitis and COVID-19. A comprehensive understanding of the immune and inflammatory mechanisms of hypertension is crucial for safely and effectively translating the findings to clinical practice., (© 2024. Springer Nature Limited.)

Introduction Obesity has became a significant health concern over the past decade. According to a higher body mass index (BMI), obesity enhances the probability of malignancy, type 2 diabetes mellitus, cardiac disorders, and musculoskeletal diseases. Bariatric surgery, a typical and effective surgical intervention for patients with excess body weight with concurrent medical conditions, achieves significant weight loss over a long period. Numerous studies have been conducted on the effectiveness of various bariatric surgery techniques for improving glycemic homeostasis and helping patients lose weight. However, little is known about how bariatric surgery affects the lipid profile. The study aims to determine how patients' altered BMI affects lipid parameters following OAGB/MGB surgery. Methods To achieve this, the longitudinal observational study was conducted from January 2021 to January 2022 among 150 patients scheduled to undergo Anastomosis Gastric Bypass Surgery. The mean age of the patients was 41.7 years, with a standard deviation of 14.7 years (mean±SD: 41.7±14.7). Among the study participants, 56 individuals (37.3%) were male, while 94 (62.7%) were female. Objectives Regarding comorbidities, hypertension was identified as the most prevalent condition among the enrolled patients, affecting 49.3% of them. Results It was observed that the levels of S. Cholesterol and S. Triglyceride showed a significant decrease after one month (Visit-1) of the bypass surgery, with a reduction of 21.8 mg/dl (95% CI=-31.9, -11.6, p=<0.001) and 14 mg/dl (95% CI=-25.5, -2.51, p=0.017), respectively Conclusion OAGB outcome is associated with a healthier lipid profile and enhanced weight management. [ABSTRACT FROM AUTHOR]

Mitochondria retain bacterial traits due to their endosymbiotic origin, but host cells do not recognize them as foreign because the organelles are sequestered. However, the regulated release of mitochondrial factors into the cytosol can trigger cell death, innate immunity and inflammation. This selective breakdown in the 2-billion-year-old endosymbiotic relationship enables mitochondria to act as intracellular signalling hubs. Mitochondrial signals include proteins, nucleic acids, phospholipids, metabolites and reactive oxygen species, which have many modes of release from mitochondria, and of decoding in the cytosol and nucleus. Because these mitochondrial signals probably contribute to the homeostatic role of inflammation, dysregulation of these processes may lead to autoimmune and inflammatory diseases. A potential reason for the increased incidence of these diseases may be changes in mitochondrial function and signalling in response to such recent phenomena as obesity, dietary changes and other environmental factors. Focusing on the mixed heritage of mitochondria therefore leads to predictions for future insights, research paths and therapeutic opportunities. Thus, whereas mitochondria can be considered 'the enemy within' the cell, evolution has used this strained relationship in intriguing ways, with increasing evidence pointing to the recent failure of endosymbiosis being critical for the pathogenesis of inflammatory diseases., (© 2024. Springer Nature Limited.)

Background: Several studies have shown that the intake of N. sativa has a beneficial effect on metabolic syndrome and related disorders. In this meta-analysis, our primary objective was to assess the impact of Nigella sativa consumption on inflammation and oxidative stress biomarkers among individuals diagnosed with metabolic syndrome and its associated conditions., Methods: Our search was conducted on prominent online databases such as Web of Science, Scopus, PubMed, and EMBASE, utilizing relevant keywords until August 2023., Results: This meta-analysis was performed on 16 RCTs comprising 1033 participants. Our results showed that intake of Nigella sativa significantly decreased CRP (SMD: -0.60; (95% CI: from -0.96 to -0.23); P = 0.00), TNF-α (SMD: -0.53; (95% CI: from -0.74 to -0.53); P = 0.00); IL-6 (SMD: -0.54 ; (95% CI: from -1.01 to -0.07); P = 0.02), and MDA: (SMD: -1.28; (95% CI: from -2.11 to -0.46); P = 0.00) levels. In addition, SOD: (SMD: 1.35; (95% CI, from 0.77 to 1.93); P = 0.00) and TAC (SMD: 2.82; (95% CI, from 0.55 to 5.084); P = 0.01) levels significantly increased in the intervention group compared to the placebo group., Conclusion: Our results showed that THE consumption of N. sativa could be associated with improved oxidative stress and inflammation in patients with metabolic syndrome and related disorders., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are serious respiratory disorders caused by a variety of intrapulmonary and extrapulmonary factors. Their incidence is increasing year by year, with high morbidity and mortality rates and lack of effective treatment. Inflammation plays a crucial role in ALI development, with sphingosine kinase 1 (SphK1) being a pivotal enzyme influencing sphingolipid metabolism and participating in inflammatory responses. However, the specific impact and the signaling pathway underlying SphK1 in lipopolysaccharide (LPS)-induced ALI/ARDS are poorly understood. This investigation aimed to explore the influence of SphK1 on inflammation and delve into the mechanistic aspects of inflammation in RAW 264.7 cells during LPS-induced ALI, which is of great importance in providing new targets and strategies for ALI/ARDS treatment., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Nanopore protein (α-hemolysin) was used to detect sub-nanosized plastic particles leached from a PE-coated paper cup. These sub-nanosized plastic particles can increase the inflammation response of macrophages. [Display omitted] • Nanopore sensing detects sub-nanosized plastics in PE-coated paper cups. • Sub-nanosized plastic particles in paper cups were 1.8 times more detected in boiled water than in room temperature water. • Sub-nanosized and microplastic particles alter cell membrane dynamics. • Sub-nanosized plastic particles can induce inflammatory cell responses. In recent years, there has been growing global concern about environmental pollution, and the increasing use of plastic products has made microplastics a serious environmental pollutant worldwide. Accordingly, the development of microplastic detection methods and research on the harmful effects of microplastics on human health are being actively pursued. In this study, we detected particle leaching from PE-coated paper cups using label-free nanopore sensing to identify and quantify the presence of sub-nanosized plastic particles. Plastic particles leached from the paper cups were classified as < 1 nm and > 1 nm, and their interactions with artificial cell membranes and inflammatory responses in the cells were evaluated. The results demonstrated that in a commonly used paper cup, particles < 1.4 nm were present at a concentration of approximately 1.13 mM in hot water and 0.62 mM in room-temperature water. It was demonstrated that plastic particles < 1 nm could condense the artificial cell membrane, whereas particles > 1 nm could thicken the artificial cell membrane. Furthermore, both size ranges of particles leached from the paper cups triggered an inflammatory response in the cells, with the inflammatory response increasing in proportion to the concentration and treatment time. The detection and analysis revealed the presence of sub-nanosized plastic particles in PE-coated paper cups, which are commonly used in daily life. These particles pose health threats and contribute to environmental pollution. [ABSTRACT FROM AUTHOR]

Purpose: Inflammation is thought to be a vital element in the etiology of cancer-related fatigue (CRF), and circulating blood cell parameters could be important markers of inflammatory response. However, the associations of several major blood cell counts and their derived inflammatory indices with CRF are not well described. The present study aimed to establish whether a relationship exists between the counts of three white blood cell (WBC) types, platelets, and CRF and investigate whether several systemic inflammatory indices were associated with CRF in patients with breast cancer (BC)., Methods: A cross-sectional survey was conducted with a sample of 824 patients with BC undergoing chemotherapy. The cancer fatigue scale was administered to assess CRF. Hematological indicators, including neutrophils, lymphocytes, monocytes, and platelets, were retrieved from routine blood test. Network analyses were used to examine the associations among them., Results: Among 824 participants, the mean score of CRF was (27 ± 10), ranging from 0 to 57. The results of network models indicated that physical fatigue was negatively linked to lymphocyte counts (weight =  - 0.161), and affective fatigue was positively associated with neutrophil counts (weight = 0.070). Additionally, physical fatigue was positively linked to the platelet-to-lymphocyte ratio (PLR) (weight = 0.049)., Conclusion: There were preliminary associations of counts of three WBC types, platelet counts, and systemic inflammatory indices, with distinct dimensions of CRF in patients with BC. Findings provide empirical support for the cellular basis of fatigue-associated inflammatory states., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The objective of this meta-epidemiological study was to explore the impact of attrition rates on treatment effect estimates in randomised trials of chronic inflammatory diseases (CID) treated with biological and targeted synthetic disease-modifying drugs. We sampled trials from Cochrane reviews. Attrition rates and primary endpoint results were retrieved from trial publications; Odds ratios (ORs) were calculated from the odds of withdrawing in the experimental intervention compared to the control comparison groups (i.e., differential attrition), as well as the odds of achieving a clinical response (i.e., the trial outcome). Trials were combined using random effects restricted maximum likelihood meta-regression models and associations between estimates of treatment effects and attrition rates were analysed. From 37 meta-analyses, 179 trials were included, and 163 were analysed (301 randomised comparisons; n = 62,220 patients). Overall, the odds of withdrawal were lower in the experimental compared to control groups (random effects summary OR = 0.45, 95% CI, 0.41-0.50). The corresponding overall treatment effects were large (random effects summary OR = 4.43, 95% CI 3.92-4.99) with considerable heterogeneity across interventions and clinical specialties (I 2  = 85.7%). The ORs estimating treatment effect showed larger treatment benefits when the differential attrition was more prominent with more attrition in the control group (OR = 0.73, 95% CI 0.55-0.96). Higher attrition rates from the control arm are associated with larger estimated benefits of treatments with biological or targeted synthetic disease-modifying drugs in CID trials; differential attrition may affect estimates of treatment benefit in randomised trials., (© 2024 The Authors. Research Synthesis Methods published by John Wiley & Sons Ltd.)

In heavily urbanized world saturated with environmental pollutants, road traffic noise stands out as a significant factor contributing to widespread public health issues. It contributes in the development of a diverse range of non-communicable diseases, such as cardiovascular diseases, metabolic dysregulation, cognitive impairment, and neurodegenerative disorders. Although the exact mechanisms behind these non-auditory health effects remain unclear, the noise reaction model centres on the stress response to noise. When exposed to noise, the body activates the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, leading to the secretion of stress hormones like catecholamines and cortisol. Prolonged exposure to noise-induced stress results in chronic inflammation and oxidative stress. This review underscores the role of inflammation and oxidative stress in the progression of noise-induced vascular dysfunction, disruption of the circadian rhythm, accelerated aging, neuroinflammation, and changes in microbiome. Additionally, our focus is on understanding the interconnected nature of these health outcomes: These interconnected factors create a cascade effect, contributing to the accumulation of multiple risk factors that ultimately lead to severe adverse health effects., (© 2024. The Author(s).)

Objectives: The objectives of this study were to assess the effect of 8 weeks of moderate-intensity aerobic training on permeability inflammatory indicators of matrix metalloproteinases (MMPs) and specific tissue inhibitors of MMPs in female migraineurs., Methods: Female migraineurs (n = 28, age 32 ± 6) were randomised into two groups: migraine with exercise training (EXE + Mig, n = 13) and migraine without exercise training (NON-EXE + Mig, n = 15). Matched healthy women were also recruited as a healthy control group (CON, n = 15). The EXE-Mig group performed 8 weeks of aerobic training. Pre and post intervention, serum matrix metalloproteinases (MMP-2 and 9) and specific tissue inhibitors of MMPs (TIMP-1 and 2) were measured. In addition, body composition indices and VO 2max were determined., Results: Exercise training reduced serum MMP-9 in female migraineurs with between-group changes and a time x group interaction (p < 0.05). In addition, exercise training reduced the serum MMP-9/TIMP-1 ratio in female migraineurs with between-group changes and time x group interaction (p < 0.05). However, no training-induced effect was observed in serum TIMP-1, TIMP-2, MMP-2 contents (p > 0.05) and MMP-2/TIMP-2 ratio (p > 0.05). Finally, exercise training reduced body fat content, WHR and BMI, and improved VO 2max (p < 0.01)., Conclusions: Our results demonstrated beneficial effects of aerobic exercise training on some circulatory inflammation factors (MMP9, MMP-9/TIMP-1) and some health indicators in female migraineurs, suggesting that such training can be employed as a non-pharmacological therapeutic method., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Childhood epilepsy affects up to 1 % of children. It has been shown that 30 % of patients are resistant to drug treatments, making further investigation of other potential treatment strategies necessary. One such approach is the ketogenic diet (KD) showing promising results and potential benefits beyond the use of current antiepileptic drugs. This study aims to investigate the effects of KD on inflammation and oxidative stress, as one of the main suggested mechanisms of neuroprotection, in children with epilepsy. This narrative review was conducted using the Medline and Google Scholar databases, and by searching epilepsy, drug-resistant epilepsy, child, children, ketogenic, ketogenic diet, diet, ketogenic, keto, ketone bodies (BHB), PUFA, gut microbiota, inflammation, inflammation mediators, neurogenic inflammation, neuroinflammation, inflammatory marker, adenosine modulation, mitochondrial function, MTOR pathway, Nrf2 pathway, mitochondrial dysfunction, PPARɣ, oxidative stress, ROS/RNS, and stress oxidative as keywords. Compelling evidence underscores inflammation and oxidative stress as pivotal factors in epilepsy, even in cases with genetic origins. The ketogenic diet effectively addresses these factors by reducing ROS and RNS, enhancing antioxidant defenses, improving mitochondrial function, and regulating inflammatory genes. Additionally, KD curbs pro-inflammatory cytokine and chemokine production by dampening NF-κB activation, inhibiting the NLRP3 inflammasome, increasing brain adenosine levels, mTOR pathway inhibition, upregulating PPARɣ expression, and promoting a healthy gut microbiota while emphasizing the consumption of healthy fats. KD could be considered a promising therapeutic intervention in patients with epilepsy particularly in drug-resistant epilepsy cases, due to its targeted approach addressing oxidative stress and inflammatory mechanisms., (© 2024 Walter de Gruyter GmbH, Berlin/Boston.)

• Remote dried blood spot (DBS) self-collection in older adults is highly feasible. • Remote DBS yields high-quality spots, sufficient for assaying multiple biomarkers, with high participant adherence. • Inflammatory markers (CRP, IL-6, TNF-α) from self-collected DBS are reliable and valid. Dried blood spots (DBS) provide a minimally invasive method to assess inflammatory markers and can be collected remotely at-home or in-person in the lab. However, there is a lack of methodological information comparing these different collection methods and in older adults. We investigated the feasibility (including adherence, yield, quality, and participant preferences) and measurement properties (reliability, validity) of remotely collected DBS inflammatory markers in older adults. Participants (N = 167, mean age = 72, range: 60–96 years) collected their own DBS (finger prick on filter paper) during three remote interviews over ∼ 6 months. Within 4–5 days on average of their last remote interview, a subset of 41 participants also attended an in-person lab visit that included a researcher-collected DBS sample, venous blood draw, and survey to assess participant preferences of DBS collection. DBS and venous blood were assayed for CRP, IL-6, and TNF-α. Adherence: 98% of expected DBS samples (493 out of 501) were completed and mailed back to the lab. Yield: 97% of DBS samples were sufficient for all assays. Quality: On average, 0.80 fewer optimal spots (60uL of blood that filled the entire circle) were obtained remotely vs. in-person (p = 0.013), but the number of useable or better spots (at least 30-40uL of blood) did not differ (p = 0.89). Preference: A slight majority of participants (54%) preferred in-person DBS collection. Reliability: DBS test–retest reliabilities were good: CRP (ICC = 0.74), IL-6 (ICC = 0.76), and TNF-α (ICC = 0.70). Validity: Inflammatory levels from DBS correlated strongly with levels from venous blood (r = 0.60-0.99) and correlated as expected with sociodemographic and physical health and function variables. Older adults can remotely collect their own DBS to acquire reliable and valid inflammatory data. Remote DBS collection is highly feasible and may allow for inflammatory markers to be assessed in larger, more representative samples than are possible with lab- or clinic-based research designs. [ABSTRACT FROM AUTHOR]

Background: Spinal cord injury (SCI) is a nervous system disease leading to motor and sensory dysfunction below the injury level, and can result in paralysis. MicroRNAs (miRNAs) play a key role in SCI treatment, and related research provides insights for SCI diagnosis and treatment. Bibliometrics is an important tool for literature statistics and evaluation, objectively summarizing multidimensional information. This study comprehensively overviews the field through bibliometric analysis of miRNA and SCI research, providing contemporary resources for future collaboration and clinical treatment. Materials and methods: In this study, we searched the Web of Science Core Collection (WOSCC) database. After careful screening and data import, we extracted annual publications, citation counts, countries, institutions, authors, journals, highly cited articles, co-cited articles, keywords, and H-index. Bibliometrics and visualization analyses employed VOSviewer, CiteSpace, the R package "bibliometrix," and online analytic platforms. Using Arrowsmith, 1 we determined miRNA-SCI relationships and discussed potential miRNA mechanisms in SCI. Results: From 2008 to 2024, the number of related papers increased annually, reaching 754. The number of yearly publications remained high and entered a period of rapid development. Researchers from 50 countries/regions, 802 institutions, 278 journals, and 3,867 authors participated in the field. Currently, China has advantages in the number of national papers, citations, institutions, and authors. However, it is necessary to strengthen cooperation among different authors, institutions, and countries to promote the production of important academic achievements. The research in the field currently focuses on nerve injury, apoptosis, and gene expression. Future research directions mainly involve molecular mechanisms, clinical trials, exosomes, and inflammatory reactions. Conclusion: Overall, this study comprehensively analyzes the research status and frontier of miRNAs in SCI. A systematic summary provides a complete and intuitive understanding of the relationship between SCI and miRNAs. The presented findings establish a basis for future research and clinical application in this field. [ABSTRACT FROM AUTHOR]

BioGlue is one of the best-known substances used as a tissue adhesive during surgical procedures, especially in cardiac surgery. Inappropriate use of BioGlue can result in inflammation in both the heart and adjacent tissues after its intraoperative application. Inflammation caused by BioGlue in cardiac surgery is a topic that has been discussed by numerous authors in scientific studies, meta-analyses and evaluations of this tissue adhesive. However, there is a lack of collected knowledge on this subject in a single concise article. The purpose of this paper is to review the current medical knowledge on the use of BioGlue in cardiac surgery versus the induction of an inflammatory response. Our paper discusses the details of this problem according to the most recent scientific reports. [ABSTRACT FROM AUTHOR]

Pueraria is a time-honored food and medicinal plant, which is widely used in China. Puerarin, the main component extracted from pueraria, has a variety of pharmacological characteristics. In recent years, puerarin has received increasing attention for its significant hepatoprotective effects, such as metabolic dysfunction-associated steatotic liver disease, alcohol-related liver disease, and hepatic carcinoma. This paper explores the pharmacological effects of puerarin on various liver diseases through multiple mechanisms, including inflammation factors, oxidative stress, lipid metabolism, apoptosis, and autophagy. Due to its restricted solubility, pharmacokinetic studies revealed that puerarin has a low bioavailability. However, combining puerarin with novel drug delivery systems can improve its bioavailability. Meanwhile, puerarin has very low toxicity and high safety, providing a solid foundation for its further. In addition, this paper discusses puerarin's clinical trials, highlighting its unique advantages. Given its excellent pharmacological effects, puerarin is expected to be a potential drug for the treatment of various liver diseases. [ABSTRACT FROM AUTHOR]

Background: Prostate cancer (PCa) is the second most prevalent malignancy among men globally. The diagnosis, treatment, and prognosis of prostate cancer frequently fall short of expectations. In recent years, the connection between inflammation and prostate cancer has attracted considerable attention. However, there is a lack of bibliometric studies analyzing the research on inflammation within the domain of prostate cancer. Research methods: We utilized the Web of Science Core Collection (WOSCC) as our data source to extract articles and reviews related to inflammation in prostate cancer, published up until April 12, 2024. The collected data underwent meticulous manual screening, followed by bibliometric analysis and visualization using the Biblioshiny package in R. Results: This study encompasses an analysis of 2,786 papers focusing on inflammation-related research within the realm of prostate cancer. Recent years have seen a significant proliferation of publications in this area, with the United States and China being the foremost contributors. The most prolific author in this domain is Demarzoam, with Johns Hopkins University standing out as the most influential institution. The leading journal in disseminating these studies is PROSTATE. Keyword co-occurrence analysis reveals that ‘inflammation-related biomarkers’, ‘inflammation index’, and ‘tumor immune microenvironment’ represent the current research hotspots and frontiers. Conclusion: The findings of this bibliometric study serve to illuminate the current landscape of inflammation-related research in the field of prostate cancer, while further augmenting the discourse on inflammation-mediated cancer therapeutics. Of particular note is the potential of these discoveries to facilitate a more nuanced understanding among researchers regarding the interplay between inflammation and prostate cancer. [ABSTRACT FROM AUTHOR]

Intervertebral disc degeneration (IDD) serves as the underlying pathology for various spinal degenerative conditions and is a primary contributor to low back pain (LBP). Recent studies have revealed a strong correlation between IDD and biological processes such as Programmed Cell Death (PCD), cellular senescence, inflammation, cell proliferation, extracellular matrix (ECM) degradation, and oxidative stress (OS). Of particular interest is the emerging evidence highlighting the significant involvement of the JNK signaling pathway in these fundamental biological processes of IDD. This paper explores the potential mechanisms through the JNK signaling pathway influences IDD in diverse ways. The objective of this article is to offer a fresh perspective and methodology for in-depth investigation into the pathogenesis of IDD by thoroughly examining the interplay between the JNK signaling pathway and IDD. Moreover, this paper summarizes the drugs and natural compounds that alleviate the progression of IDD by regulating the JNK signaling pathway. This paper aims to identify potential therapeutic targets and strategies for IDD treatment, providing valuable insights for clinical application. [ABSTRACT FROM AUTHOR]

Simple Summary: Rare diseases represent a significant health problem since patients face difficulty obtaining a rapid diagnosis and a proper treatment. An inflammatory pseudotumor of the liver (IPTL) is a rare and benign entity in which reaching a correct preoperative diagnosis can be challenging since it is similar to the worst form of liver cancer, intrahepatic cholangiocarcinoma (ICC). Our paper aims to report our experience and to review the available literature on this topic, thus summarizing previous experiences and central issues to point out a prompt road map of treatment that still needs to be standardized. IPTL is not associated with substantial risk factors and presents with faint symptoms. Imaging data via MRI and CT scan are not specific, thus often requiring ultrasound (US)-guided biopsy. Proper and widely accepted gold standard treatment does not exist; conservative strategies represent an accepted option, while the decision for surgery still exists where there is a suspicion of malignancy. An inflammatory pseudotumor of the liver is a rare tumor-like lesion composed of polymorphous inflammatory cell infiltrates and variable amounts of fibrosis that can often mimic a malignant liver neoplasm. The etiology of inflammatory pseudotumors of the liver is unknown; symptoms are faint and imaging non-specific. Thus, it is often hard to make a diagnosis preoperatively and it is not so rare to over-treat patients with this disease or vice versa. Thus, more profound knowledge is necessary to plan appropriate disease management. We reported our two cases and systematically searched the literature regarding IPTL. We selected articles published in English from four databases, PubMed, Scopus, Web of Science and Google Scholar, and we included only articles with consistent data. Twenty nine papers fulfilling criteria for the review were selected. The analysis of 69 cases published from 1953 confirmed that the risk factors are unclear, the imaging data is not specific, and biopsy is crucial but not so widely used in clinical practice due to the procedure's related risks, and relatively low effectiveness and improvement in imaging analysis. Regarding treatment, surgeons have moved towards a more conservative attitude over the years due to better imaging quality and patient surveillance. However, surgery remains the modality of choice for most cases with an indeterminate diagnosis. Even if an inflammatory pseudotumor of the liver is a benign tumor with a good prognosis, not requiring any treatment in most cases, sometimes it remains challenging to differentiate it from ICC; therefore, there is a solid recommendation to manage this condition with a multidisciplinary team. [ABSTRACT FROM AUTHOR]

Systematic inflammatory response syndrome (SIRS) and the accompanying sepsis pose a huge threat to human health worldwide. Heparin is a part of the standard supportive care for the disease. However, the molecular mechanism is not fully understood yet, and the potential signaling pathways that play key roles have not yet been elucidated. In this paper, the main findings regarding the molecular mechanisms associated with the beneficial effects of heparin, including inhibiting HMGB-1-driven inflammation reactions, histone-induced toxicity, thrombo-inflammatory response control and the new emerging mechanisms are concluded. To set up the link between the preclinical research and the clinical effects, the outcomes of the clinical trials are summarized. Then, the structure and function relationship of heparin is discussed. By providing an updated analysis of the above results, the paper highlights the feasibility of heparin as a possible alternative for sepsis prophylaxis and therapy. [ABSTRACT FROM AUTHOR]

Background: Aging has been implicated in many chronic inflammatory diseases, including periodontitis. Periodontitis is an inflammatory disease caused by longterm irritation of the periodontal tissues by the plaque biofilm on the surface of the teeth. However, only a few bibliometric analyses have systematically studied this field to date. This work sought to visualize research hot spots and trends in aging associated with periodontitis from 2002 to 2023 through bibliometric approaches. Methods: Graphpad prism v8.0.2 was used to analyse and plot annual papers, national publication trends and national publication heat maps. In addition, CtieSpace (6.1.6R (64-bit) Advanced Edition) and VOSviewer (version 1.6.18) were used to analyse these data and visualize the scientific knowledge graph. Results: The number of documents related to aging associated with periodontitis has steadily increased over 21 years. With six of the top ten institutions in terms of publications coming from the US, the US is a major driver of research in this area. journal of periodontology is the most published journal in the field. Tonetti MS is the most prolific authors and co-cited authors in the field. Journal of Periodontology and Journal of Clinical Periodontology are the most popular journals in the field with the largest literature. Periodontitis, Alzheimer's disease, and peri-implantitis are current hot topics and trends in the field. Inflammation, biomarkers, oxidative stress cytokines are current research hotspots in this field. Conclusion: Our research found that global publications regarding research on aging associated with periodontitis increased dramatically and were expected to continue increasing. Inflammation and aging, and the relationship between periodontitis and systemic diseases, are topics worthy of attention. [ABSTRACT FROM AUTHOR]

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Purpose: Chronic inflammation is one of the key mechanisms of depression. Wenyang-Tianjin-Jie Decoction (WTJD) is an effective antidepressant found in the course of diagnosis and treatment, but the mechanism of therapeutic effect is not clear. The study aimed to evaluate the efficacy of WTJD in the kidney yang deficiency (KYD) type of depression rats and reveal its mechanisms. Materials and Methods: We selected forty 6-week-old male Sprague-Dawley rats for the study. We established a KYD [Phellodendron amurense Rupr (Huangbai) solution oral gavage and 4°C environments; 8 weeks] type of depression (chronic unpredictable mild stimulus; 6 weeks) rat model first. After successful modeling, we used WTJD or fluoxetine on rats for 3 weeks. Then we evaluated the depression and KYD behavior. Finally, we observed the expression of key inflammatory factors and proteins in peripheral blood and hippocampus, and further investigated the immune balance of Th17/Treg and Th1/Th2 cells and the activity of their main regulatory pathways JAK2/STAT3 and TLR4/TRAF6/NF-κB. Results: The imbalance of Th17/Treg and Th1/Th2 cells in rats were related to KYD and depressive symptoms. Through this study, we found that WTJD can inhibit the activity of JAK2/STAT3 and TLR4/TRAF6/NF-κB pathways, balance Th17/Treg and Th1/Th2 cell homeostasis, regulate the levels of inflammatory factors in the hippocampus and peripheral blood, and reverse KYD and depression. Conclusion: This study confirmed that WTJD had a reliable effect on depression rats with KYD, and its mechanism was to regulate the immune homeostasis of hippocampal T cells and related inflammatory factors to improve KYD and depression symptoms in rats. [ABSTRACT FROM AUTHOR]

The article focuses on long COVID, a multi-system condition following SARS-CoV-2 infection, and highlights that while it predominantly affects adults, it can also impact children and adolescents, with milder severity and shorter duration possibly attributed to protective factors.

Simple Summary: Myeloid-derived suppressor cells (MDSCs) are immature cells that expand in the circulation of patients with cancer, sepsis or chronic inflammation, modulate the immune response against cancer (favoring tumor onset and progression) and promote neoangiogenesis. These premises suggest that MDSCs could be involved in the pathogenesis of primary myelofibrosis (PMF) (a myeloproliferative neoplasm characterized by chronic inflammation and extensive neoangiogenesis in bone marrow and spleen). In this paper, we found that (1) MDSCs are increased both in the circulation and in the spleen of PMF patients and strongly correlate with disease progression; and (2) reduced CXCR4 expression on MDSCs along with increased plasmatic SDF-1α can be involved in their mobilization. These findings suggest that circulating MDSCs can be considered a parameter of disease severity and set MDSCs as potential new targets for cancer therapy. Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by a chronic inflammatory state that plays a relevant role in the disease pathogenesis (as proven by high levels of inflammatory cytokines with prognostic significance and by a persistent oxidative stress) and by extensive neoangiogenesis in bone marrow (BM) and spleen. Myeloid-derived suppressor cells (MDSCs) are immature cells that expand in patients with cancer, sepsis or chronic inflammation, favoring tumor onset and progression mainly through the decrease in immune surveillance and the promotion of neoangiogenesis. In this paper, we evaluated the presence of circulating MDSCs in PMF patients, the plasmatic factors involved in their mobilization/expansion and the correlations with laboratory, genetic and clinical parameters. The data indicated that MDSCs could have a relevant role in PMF as a new pathogenic mechanism contributing to explaining the phenotypic diversity observed during the clinical course of the disease, or a potential new target for personalized treatment. [ABSTRACT FROM AUTHOR]

Simple Summary: Achieving improved rates of overall survival remains a significant challenge in advanced-stage ovarian cancer; even if complete debulking is achieved, certain patients report poor results in terms of survival. Therefore, the aim of this paper is to investigate new prognostic markers that could point out which cases could benefit most from debulking surgery and which ones should be rather submitted to neoadjuvant therapies followed by debulking surgery. Background: Despite improving surgical techniques and achieving more often complete debulking procedures, certain patients with advanced-stage ovarian cancer still have a very poor prognosis. The aim of the current paper is to investigate whether inflammatory and nutritional status can predict the long-term outcomes of ovarian cancer patients. Methods: A retrospective analysis of 57 cases diagnosed with advanced-stage ovarian cancer submitted to surgery as first intent therapy was carried out. In all cases, the preoperative status was determined by calculating the CRP/albumin ratio, as well as the Glasgow score, the modified Glasgow score and the prognostic nutritional index. Results: Patients presenting higher values of the CRP/albumin ratio, with a higher Glasgow score, modified Glasgow score and prognostic nutritional index (PNI), were more frequently associated with incomplete debulking surgery, a higher peritoneal carcinomatosis index and poorer overall survival (20 months versus 9 months for the CRP/albumin ratio p = 0.011, 42 versus 27 versus 12 months for the Glasgow score p = 0.042, 50 versus 19 versus 12 months for the modified Glasgow score, p = 0.001, and 54 months versus 21 months, p = 0.011 for the prognostic nutritional index). Conclusions: A strong relationship between the nutritional and inflammatory status in advanced-stage ovarian cancer seems to exist. [ABSTRACT FROM AUTHOR]

Major depressive disorder (MDD) is a severe psychiatric illness known to be highly complex due to its difficulty in identifying genetic factors and its polygenic nature. While genetic studies and research into epigenetic changes have advanced our understanding of MDD, the precise role of genetics in MDD's manifestation remains elusive. This paper reviews the current state of research on MDD genetics, encompassing findings on MDD's biological blueprint and investigations into epigenetic modifications associated with MDD development. Furthermore, this paper explores the interplay between depression and the immune system and the impact of inflammation on the disorder. Neuroimaging studies have also impacted comprehension of MDD, revealing alterations in brain size and chemistry. These insights shed light on the biological underpinnings of MDD and hold promise for developing more effective treatments and therapies for patients. [ABSTRACT FROM AUTHOR]

Periapical periodontitis is a chronic inflammatory disease, caused by endodontic infection, and its development is regulated by the host immune/inflammatory response. Metabolic disorders, which are largely dependent on life style such as eating habits, have been interpreted as a "metabolically-triggered" low-grade systemic inflammation and may interact with periapical periodontitis by triggering immune modulation. Diabetes mellitus (DM) is a group of complex multisystem metabolic disorders due to a deficiency in insulin secretion caused by pancreatic ß-cell dysfunction and/or insulin resistance in liver and muscle. Objective: In this paper, the current status of knowledge regarding the relationship between periapical inflammation and diabetes mellitus type II is reviewed. Material and method: Research was conducted on scientific papers published on Medline - Pub med in the past 10 years (from 2012-2022). The search was performed using the Mesh (Medical Subject Headings) key words: periapical inflammatory lesions, periapical periodontitis and diabetes mellitus type II. Results: Several studies have analyzed the possible association between periapical inflammatory lesions and diabetes mellitus type II. The results of studies carried mainly in animal models, less in humans suggested association between endodontic variables such as apical periodontitis, root canal treatment and diabetes mellitus type 2. The demonstration of association does not prove by itself the existence of a cause-effect relationship. Conclusion: A review of the literature showed connection between periapical inflammatory lesions and diabetes mellitus type II, but prospective case control clinical studies are needed for further clarifying this relation. [ABSTRACT FROM AUTHOR]

Although antiviral drugs can effectively inhibit hepatitis B virus (HBV) replication, the maintenance of chronic inflammation in the liver is still considered to be an important cause for the progression of HBV-related liver disease to liver fibrosis and advanced liver disease. As an endogenous inhibitory receptor of IL-1R and TLR signaling pathways, single immunoglobulin interleukin-1-related receptor (SIGIRR) has been proven to reduce inflammation in tissues to maintain system homeostasis. However, the relationship between SIGIRR expression and HBV replication and inflammatory pathway activation in hepatocytes remains unclear. In this study, hepatitis B virus X protein (HBx) upregulated MyD88 in liver cells, promoting NF-κB signaling and inflammatory factor production with LPS treatment, and the cell supernatant accelerated the activation and collagen secretion of hepatic stellate cells. However, SIGIRR overexpression suppressed HBx-mediated MyD88/NF-κB inflammatory signaling activation and inflammatory cytokine production induced by LPS in hepatocytes and HBV replication hepatocytes. Although we did not find any effect of SIGIRR on HBV replication in vitro, this study investigated the role of SIGIRR in blocking the proinflammatory function of HBx, which may provide a new idea for the treatment of chronic hepatitis B., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Per- and polyfluoroalkyl substances (PFAS) pose potential risks to human health. In real-world settings, humans are exposed to various PFAS through numerous pathways., Objectives: This study evaluated the associations between co-exposure to PFAS and obesity and its comorbidities, along with the mediating roles of inflammation and oxidative stress., Methods: We analyzed 11,090 participants from National Health and Nutrition Examination Survey (NHANES), 2003-2018. Linear regression, logistic regression, and generalized additive models were used to assess the individual effects of PFAS exposure on obesity and its comorbidities. The environmental risk score (ERS) was calculated using the adaptive elastic-net model to assess the co-exposure effects. Linear and logistic regression models explored the associations between ERS and obesity and its comorbidities. Mediation analyses explored the roles of inflammatory (neutrophils, lymphocytes, and alkaline phosphatase) and oxidative stress (gamma-glutamyl transferase, total bilirubin, and uric acid) markers in the associations between ERS and obesity and its comorbidities., Results: For each unit increase in ERS, the odds of obesity and type 2 diabetes mellitus (T2DM) increased 3.60-fold (95 % CI: 2.03, 6.38) and 1.91-fold (95 % CI: 1.28, 2.86), respectively. For each unit increase in ERS, BMI increased by 2.36 (95 % CI: 1.24, 3.48) kg/m 2 , waist circumference increased by 6.47 (95 % CI: 3.56, 9.37) cm, and waist-to-height ratio increased by 0.04 (95 % CI: 0.02, 0.06). Lymphocytes, alkaline phosphatase, and total bilirubin were significantly associated with both ERS and obesity, with mediation proportions of 4.17 %, 3.62 %, and 7.37 %, respectively. Lymphocytes, alkaline phosphatase, total bilirubin, and uric acid were significantly associated with both ERS and T2DM, with the mediation proportions of 8.90 %, 8.74 %, 29.73 %, and 38.19 %, respectively., Conclusions: Co-exposure to PFAS was associated with obesity and T2DM, and these associations may be mediated by inflammation and oxidative stress. Further mechanistic and prospective studies are required to verify these associations., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Osteoarthritis is a prevalent musculoskeletal disease that involves cartilage degradation, subchondral bone remodeling, and synovial inflammation and ultimately causes physical disability. Common risk factors for osteoarthritis include age, sex, obesity, and genetic predispositions. Treatment includes nonpharmaceutical and pharmacological approaches; however, disease-modifying osteoarthritis drugs remain undeveloped. We aimed to identify key regulatory factors underlying the etiology of osteoarthritis. We studied alterations of the inflammatory responses after manipulating the expression of MTLN, which we selected after sequencing and transcriptomics of the patients' synovial tissues. MTLN expression was increased in synovial tissues of patients and in SW982 human synovial sarcoma cells following inflammatory stimuli. We found that MTLN overexpression or knockout respectively decreased or increased expression of the inflammation-associated genes, including IL-6, IL-8, and TNF-α. Thus, high levels of MTLN in osteoarthritis may protect tissues against excessive inflammation, thereby offering therapeutic potentials., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Immune-mediated inflammatory disease (IMID) is a complex disorder characterized by excessive immune responses involving T cells and their subsets, leading to direct tissue damage. T cells can be broadly categorized into CD4 + T cells and CD8 + T cells. CD4 + T cells are composed of several subsets, including T helper (Th)1, Th2, Th9, Th17, Th22, follicular helper T cells (Tfhs), and regulatory T cells (Tregs), while effector CD8 + T cells consist mainly of cytotoxic T cells (CTLs). Current therapies for IMID are ineffective, prompting exploration into mesenchymal stem cells (MSCs) as a promising clinical treatment due to their immunomodulatory effects and self-renewal potential. Recent studies have shown that MSCs can suppress T cells through direct cell-to-cell contact or secretion of soluble cytokines. Nevertheless, the precise effects of MSCs on T cell subsets remain inadequately defined. In this review, we summarize the most recent studies that have examined how MSCs modulate one or more effector T-cell subsets and the mechanisms behind these modifications in vitro and several mouse models of clinical inflammation. This also provides theoretical support and novel insights into the efficacy of clinical treatments involving MSCs. However, the efficacy of MSC therapies in clinical models of inflammation varies, showing effective remission in most cases, but also with exacerbation of T-cell-mediated inflammatory damage in some instances., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Sun li reports financial support was provided by Jiangsu National Natural Science Foundation and National Natural Science Foundation of China. Zhu wei reports financial support was provided by National Natural Science Foundation of China. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Acute kidney injury (AKI) is a severe medical condition that can lead to illness and death. A disintegrin and metalloprotease (ADAM) protein family is a potential treatment target for AKI due to its involvement in inflammation, growth, and differentiation. While ADAM10 and ADAM17 have been identified as significant contributors to inflammation, it is unclear whether they play a critical role in AKI. In this study, we induced AKI in male and female mice using lipopolysaccharide, a bacterial endotoxin that causes inflammation and oxidative stress. The role of kaempferol, which is found in many natural products and known to have antioxidant and anti-inflammatory activity in many pre-clinical studies, was investigated through ADAM10/17 enzymes in AKI. We also investigated the efficacy of a selective synthetic inhibitor named GW280264X for ADAM10/17 inhibition in AKI. Blood urea nitrogen and creatinine levels were measured in serum, while tumor necrosis factor-α, vascular adhesion molecule, interleukin (IL)-1β, glucose regulatory protein-78, IL-10, nuclear factor κ-B, thiobarbituric acid reactive substances, total thiol, ADAM10, and ADAM17 levels were measured in kidney tissue. We also evaluated kidney tissue histologically using hematoxylin and eosin, periodic acid-schiff, and caspase-3 staining. This research demonstrates that GW280264X and kaempferol reduces inflammation and oxidative stress, as evidenced by biochemical and histopathological results in AKI through ADAM10/17 inhibition. These findings suggest that inhibiting ADAM10/17 may be a promising therapeutic approach for treating acute kidney injury., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Inflammation is a protective mechanism against endogenous and exogenous pathogens. It is a typical feature of numerous chronic diseases and their complications. Keap1 is an essential target in oxidative stress and inflammatory diseases. Among them, the Keap1-Nrf2-ARE pathway (including Keap1-Nrf2-HO-1) is the most significant pathway of Keap1 targets, which participates in the control of inflammation in multiple organs (including renal inflammation, lung inflammation, liver inflammation, neuroinflammation, etc.). Identifying new Keap1 inhibitors is crucial for new drug discovery. However, most drugs have specificity issues as they covalently bind to cysteine residues of Keap1, causing off-target effects. Therefore, direct inhibition of Keap1-Nrf2 PPIs is a new research idea. Through non-electrophilic and non-covalent binding, its inhibitors have better specificity and ability to activate Nrf2, and targeting therapy against Keap1-Nrf2 PPIs has become a new method for drug development in chronic diseases. This review summarizes the members and downstream genes of the Keap1-related pathway and their roles in inflammatory disease models. In addition, we summarize all the research progress of anti-inflammatory drugs targeting Keap1 from 2010 to 2024, mainly describing their biological functions, molecular mechanisms of action, and therapeutic roles in inflammatory diseases., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Noise and air pollution are significant environmental threats with proven adverse health effects. However, the causality between these ambient exposures and disease is still largely unknown. This study aims to provide genetic evidence for this gap and investigates the dual role of inflammatory factors, emphasizing the need for integrated public health strategies., Methods: We included noise and air pollution as exposures, 91 inflammatory factors as mediators, and 26 diseases as outcomes. We explored causal relationships using Mendelian randomization. To ensure the reliability, we screened single nucleotide polymorphisms (SNPs) closely associated with exposure as instrumental variables (IVs), and assessed the pleiotropy and heterogeneity of these IVs., Results: Our results suggest that "Hearing difficulty/problems with background noise" increases the risk of hypertension, bronchitis, and menopause; loud music exposure frequency increases the risk of bronchitis; noisy workplace raises the risk of hypertension, coronary heart disease, narcolepsy, and irritable bowel syndrome; NO 2 increases the risk of myocardial infarction and chronic heart failure; NO x increases the risk of pneumonia and inflammatory diseases of female pelvic organs; and PM 10 increases the risk of myocardial infarction, narcolepsy, and type 2 diabetes; PM 2.5 - 10 increases the risk of developing pneumonia and type 2 diabetes. Furthermore, we found that nine inflammatory factors play a mediating role, of which four play a mediating role in increasing the risk of morbidity and eight play a mediating role in protection against ambient exposures. Finally, we selected SNPs significantly associated with exposure and outcome for enrichment analysis., Conclusions: This study provides the first genetic evidence linking noise and air pollution to various diseases, highlighting the dual mediating role of inflammatory factors. Our findings align with the "One Health" framework, emphasizing the interconnectedness of environmental and human health. Integrated public health strategies considering these complex biological responses are essential for promoting overall well-being., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: The nasopharynx serves as a crucial niche for the microbiome of the upper respiratory tract. However, the association between the intratumoral microbiota and host systemic inflammation and immune status in nasopharyngeal carcinoma (NPC) remain uncertain., Methods: We performed 5R 16S rDNA sequencing on NPC tissue samples, followed by diversity analysis, LEfSe differential analysis, and KEGG functional prediction. The analyses were based on indices such as AISI, SIRI, PAR, PLR, and NAR. Correlation analyses between microbes and these indices were performed to identify microbes associated with inflammation and immune status. Additionally, regression analysis based on tumor TNM stage was performed to identify key microbes linked to tumor progression. The head and neck squamous cell carcinoma (HNSC) transcriptome and the paired HNSC microbiome data from TCGA were utilized to validate the analyses., Results: The Proteobacteria, Actinobacteria, Firmicutes, and Bacteroidetes were the most enriched phyla in NPC tissues. Microbes within these phyla demonstrated high sensitivity to changes in host systemic inflammation and immune status. Proteobacteria and Firmicutes showed significant differences between inflammation groups. Actinobacteria varied specifically with platelet-related inflammatory indices, and Bacteroidetes genera exhibited significant differences between NAR groups. Corynebacterium and Brevundimonas significantly impacted the T stage of tumors, with a high load of Corynebacterium within tumors associated with a better prognosis CONCLUSION: Our analysis indicates that Proteobacteria play a crucial role in the inflammatory state of NPC, while Bacteroidetes are more sensitive to the tumor immune status., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Cardiovascular diseases (CVDs) represent a significant public health concern because of their associations with inflammation, oxidative stress, and abnormal remodeling of the heart and blood vessels. In this review, we discuss the intricate interplay between mitochondria-associated membranes (MAMs) and cardiovascular inflammation, highlighting their role in key cellular processes such as calcium homeostasis, lipid metabolism, oxidative stress management, and ERS. We explored how these functions impact the pathogenesis and progression of various CVDs, including myocardial ischemia-reperfusion injury, atherosclerosis, diabetic cardiomyopathy, cardiovascular aging, heart failure, and pulmonary hypertension. Additionally, we examined current therapeutic strategies targeting MAM-related pathways and proteins, emphasizing the potential of MAMs as therapeutic targets. Our review aims to provide new insights into the mechanisms of cardiovascular inflammation and propose novel therapeutic approaches to improve cardiovascular health outcomes., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Ethnopharmacological Relevance: Tagetes erecta L. (Asteraceae), popularly known as Aztec Marigold, is used in folk medicine to treat several ailments including inflammatory processes. Despite its historical use, the specific mechanisms through which it may modulate inflammation, particularly its effects on neutrophils and macrophages activation, have not yet been completely investigated., Aim of the Study: This study aimed to elucidate the anti-inflammatory mechanism of the hydroalcoholic extract obtained from T. erecta flowers, focusing on its role in the regulation of neutrophil and macrophage functions., Material and Methods: The production of TNF, IL-6, CXCL-1, IL-1β, IL-10 (ELISA) and NO (Griess reaction), adhesion molecule expression (CD62L, CD49d and CD18, flow cytometry), and chemotaxis were analyzed in vitro using oyster glycogen-recruited peritoneal neutrophils or macrophages (RAW 264.7) stimulated with lipopolysaccharide (LPS) and treated with the extract (1, 10 or 100 μg/mL). The resolution of inflammation was accessed by efferocytosis assay. The in vivo anti-inflammatory activity was investigated using carrageenan-induced inflammation in the subcutaneous tissue of male Swiss mice orally treated with the T. erecta extract (30, 100 or 300 mg/kg). The leukocyte influx (optical microscopy), secretion of chemical mediators (TNF, IL-6 and IL-1β, ELISA) and protein exudation (Bradford reaction) were quantified in the inflamed exudate., Results: In vitro studies demonstrated that the extract inhibited neutrophil chemotaxis and reduced the production and/or release of cytokines (TNF, IL-1β, CXCL1, and IL-6) as well as nitric oxide (NO) by neutrophils and macrophages when stimulated with LPS. Neutrophils treated with LPS and incubated with the extract showed an increase in CD62L expression, which leads to the impairment of neutrophil adhesion. The extract also enhanced efferocytosis of apoptotic neutrophils by macrophages, which was accompanied by increased IL-10 secretion and decreased TNF levels. In vivo studies yielded similar results, showing reduction in neutrophil migration, protein exudation, and cytokine release (TNF, IL-6, and IL-1β)., Conclusions: Together, the data herein obtained shows that T. erecta flower extract has anti-inflammatory effects by regulating inflammatory mediators, limiting neutrophil migration, and promoting efferocytosis. The in vivo results suggest that an herbal medicine made with T. erecta could represent an interesting pharmacological tool for the treatment of acute inflammatory condition., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)