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Mushroom Phellinus linteus (" Sanghuang " in Chinese) is a popular medicinal polypore used to treat several disorders through its various biological functions. Inonotus sanghuang is claimed to produce general immune-potentiating and strengthening, anti-inflammatory, anti-tumor and anti-microbial properties, but its effect on acute lung inflammation and oxidative stress are not clearly understood. To determine the effect and mechanism of the polyphenols-rich ethyl acetate fraction from wild I. sanghuang extract (ISE) on acute lung injury (ALI) induced by bleomycin (BLM), female C57BL/6 mice were fed ISE (0%, 0.15% or 0.6% in diet) for 4 weeks prior to challenge with BLM. Bronchoalveolar lavage fluid (BALF) from lung, spleen and lung tissues were collected on day 3 after BLM challenge for histological, oxidative stress, molecular and biochemical analysis. ISE supplementation improved pathological features in lung injury scores and reduced lung wet-to-dry ratios. Moreover, ISE reduced inflammatory cell infiltration and the pro-inflammatory cytokines including IL-1β, IL-6 and TNF-α in BALF, decreased the MPO activity and the MDA level and increased the SOD, CAT and GSH-Px activities in lung tissue homogenates. Further mechanism analysis demonstrated that dietary ISE inhibited NF-κB signal. Finally, peripheral immune function analysis showed that ISE had less effect on immune response including splenocyte producing inflammatory cytokines and T cell proliferation except for IL-1β and IL-2. Our findings indicate the possibility that dietary ISE attenuates ALI induced by BLM through correcting the inflammation and oxidation balance at least in part via inhibiting NF-κB signal in vivo , suggesting that ISE might be a valuable medicinal food effective in improving lung injury. Mushroom Phellinus linteus (" Sanghuang " in Chinese) is a popular medicinal polypore and has been reported to have benefits for health. Current study showed that supplementation with a polyphenols-rich extract from wild Inonotus Sanghuang could inhibit lung inflammation and edema via anti-oxidation and anti-inflammatory effects in mice, which might be mediated at least in part via inhibiting NF-κB signal. Unlabelled Image • ISE may attenuate acute lung injury in bleomycin-treated mice. • ISE may reduce the pro-inflammatory cytokines and oxidative stress in lung tissues. • This inhibitory effect of ISE might be mediated by downregulation of NK-κB signal. • ISE has less immune-modulating effects in BLM-treated mice. [ABSTRACT FROM AUTHOR]

Background IL-37 emerges as a natural suppressor of inflammatory responses. The potential role of IL-37 in the pathology of atherosclerosis is unclear. The purpose of this study was to assess IL-37 profile in acute coronary syndrome (ACS) and the prognostic role of this cytokine in patients with ST-segment elevation acute myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). Methods In a case-control study, we prospectively enrolled 216 patients undergoing the first coronary angiography, which consisted of 5 groups: normal (n = 57), stable angina (SAP, n = 36), unstable angina (UAP, n = 42), non-STEMI (n = 36), STEMI (n = 45). Plasma IL-37, IL-6 and serum amyloid A (SAA) were measured using a commercially ELISA kit. Besides, in a prospective cohort study, 125 patients with STEMI of onset < 12 h undergoing PPCI were enrolled and divided into 2 groups according to the concentrations of IL-37 (< 341.1 pg/ml or ≥ 341.1 pg/ml). In-hospital major adverse cardiac event (MACE) including nonfatal myocardial infarction (MI), target lesion revascularization, acute heart failure, and cardiac death were estimated for prognosis. Results IL-37 was gradually increased in accordance with the severity of coronary artery disease. The circulating concentration of IL-37 was remarkably higher in the ACS patients than in either of the normal or SAP patients ( p < 0.05), and especially higher in the AMI patients including STEMI and non-STEMI than in the angina pectoris subjects no matter SAP or UAP ( p < 0.05). There was no statistical difference of IL-37 between normal and SAP patients, STEMI and non-STEMI patients ( p > 0.05). The trend of the change of IL-37 was consistent with that of SAA or IL-6. A higher circulating concentration of IL-37 before PPCI was accompanied with the decreased LVEF and the increased NT-proBNP concentrations, and independently predictive of in-hospital MACE rate in patients with STEMI undergoing PPCI (OR = 3.652, 95% CI = 1.113–11.983, p < 0.05). Conclusions We demonstrated the IL-37 profile in patients with acute coronary syndrome and the increased IL-37 concentration was associated with a worse clinical in-hospital outcome in STEMI patients undergoing PPCI. [ABSTRACT FROM AUTHOR]

Abstract: TRPA1 channels have been found to play an important role in mammalian pain sensation, especially when the pain is caused by chemicals on site of inflammation. A large number of structurally diverse chemicals are found to activate TRPA1 channels, implicating a potential chemosensor in neuronal nociception. Identification of the channel activation by cysteine modification through covalent chemical reaction provides arguments for the diversity of the agonist structures. However, it is largely unknown how nonreactive compounds activate TRPA1 channels. Here, we report that NPPB, a classic Cl− channel blocker, potently activated human TRPA1 channels overexpressed in mammalian HEK-293 cells. This effect was confirmed in Ca2+ imaging assay, patch clamp whole cell and single channel recordings. The NPPB response was quick, fully reversible and replicable, contrary to the effect of covalent modification by AITC. The mutagenesis studies revealed a refreshed look at several mutations known to be critical for the actions of AITC and menthol. The blocking profile of NPPB on these mutants showed that the NPPB activation was similar to that of FTS and different from AITC and menthol. The results indicated a possible close interaction between S5 and N-terminal domains of the channel. We also tested a group of NPPB analogs on TRPA1 channel activities. The results demonstrated that NPPB activation was tightly associated with chemical structure. None of the single chemical group was sufficient to activate the channel, indicating that NPPB activated TRPA1 through a structure-specific mechanism. [Copyright &y& Elsevier]

Bovine endometrium infection with gram-negative bacteria commonly causes uterine diseases. Previous studies indicate that prostaglandin E 2 (PGE 2) is an inflammatory mediator in bacterial endometritis. However, the mechanism underlying lipopolysaccharide (LPS)-induced inflammatory response regulation in bovine endometrial explants remains elusive. In the present study, bovine explants were pre-treated with 15-hydroxyprostaglandin dehydrogenase (15-PGDH) inhibitors before LPS stimulation. PGE 2 secretion, prostaglandin synthetase, pro-inflammatory factor, damage-associated molecular pattern (DAMP), and related signaling pathway factor levels were evaluated. Using 15-PGDH inhibitors pre-treatment, LPS-treated bovine endometrial explants exhibited augmentation of PGE 2 and DAMP expression, and upregulation of various signaling pathway factors. Protein kinase A (PKA), extracellular-signal-regulated kinase, and c-Jun N-terminal kinase phosphorylation and degradation of nuclear transcription factor-κB (NF-κB) inhibitors were induced in the pre-treated endometrial explants. The mechanism underlying LPS-induced PGE 2 accumulation acting as a pro-inflammatory mediator through toll-like receptor 4 signaling in bovine explants could involve the PKA, mitogen-activated protein kinase, and NF-κB pathways. [ABSTRACT FROM AUTHOR]

With the imbalance of intestinal microbiota, the body will then face an inflammatory response, which has serious implications for human health. Bodily allergies, injury or pathogens infections can trigger or promote inflammation and alter the intestinal environment. Meanwhile, excessive changes in the intestinal environment cause the imbalance of microbial homeostasis, which leads to the proliferation and colonization of opportunistic pathogens, invasion of the body's immune system, and the intensification of inflammation. Some natural compounds and gut microbiota and metabolites can reduce inflammation; however, the details of how they interact with the gut immune system and reduce the gut inflammatory response still need to be fully understood. The review focuses on inflammation and intestinal microbiota imbalance caused by pathogens. The body reacts differently to different types of pathogenic bacteria, and the ingestion of pathogens leads to inflamed gastrointestinal tract disorders or intestinal inflammation. In this paper, unraveling the interactions between the inflammation, pathogenic bacteria, and intestinal microbiota based on inflammation caused by several common pathogens. Finally, we summarize the effects of intestinal metabolites and natural anti-inflammatory substances on inflammation to provide help for related research of intestinal inflammation caused by pathogenic bacteria. [ABSTRACT FROM AUTHOR]

• tFNA-Que can alleviate radiation-induced oxidative stress and inflammation. • tFNA-Que presents a straightforward and efficient synergistic delivery nano-system. Radiation cystitis (RC) has impacted millions globally with high morbidity and a dearth of effective strategies. Earlier research indicated that quercetin (Que) could alleviate radiation-induced bladder damage. However, Que's limited application arises from issues such as poor water solubility, rapid degradation, and low oral bioavailability. To address these challenges, a nano-system, named tFNA-Que, has been developed for Que delivery, utilizing the tetrahedral framework nucleic acid (tFNA). Due to the anti-inflammatory, antioxidant, and delivery capabilities of tFNA, it is purposefully designed as an efficient carrier for delivering Que. The tFNA-Que formulation exhibits an easily synthesized structure, stable performance, sustained release, good water solubility, robust cellular internalization ability, desirable biocompatibility, and biosafety. As a result, tFNA-Que can alleviate radiation-induced oxidative stress and inflammation while promoting angiogenesis in RC. In summary, the synthesis of tFNA-Que presents a straightforward and efficient synergistic delivery nano-system, making it as a promising candidate for RC treatment. [ABSTRACT FROM AUTHOR]

Background Chronic obstructive pulmonary disease (COPD) concomitant with obstructive sleep apnea (OSA) is known as overlap syndrome. It has an increased rate of hospitalization due to COPD exacerbation which is believed to indicate a worsening of the underlying chronic airway inflammation. Therefore, the aim of this prospective study was to explore whether OSA exacerbates airway inflammation in subjects with COPD by examining the bronchoalveolar lavage (BAL) fluid. Methods This prospective study included 47 patients with overlap syndrome and 28 patients with moderate-to-severe stage stable COPD. Twenty-five patients with overlap syndrome adhered to the continuous positive airway pressure (CPAP) treatment; the remaining patients either refused CPAP treatment or discontinued it within two weeks owing to adverse effects or other reasons. BAL fluid was collected from all subjects for the evaluation of cell numbers and tumor necrosis factor alpha (TNFα) and interleukin-8 (IL-8) levels. Results The BAL fluid of patients with overlap syndrome showed a significantly increased proportion of neutrophils and higher TNFα concentration and IL-8 levels than that of COPD patients; however, the serum CRP levels were not significantly different. An association was found between the percentage of neutrophils and the TNFα concentration and IL-8 levels. Moreover, the TNFα concentration was significantly correlated with the percentage of nighttime spent with oxygen saturation less than 90%. After CPAP treatment, airway inflammation was found to decrease significantly. Conclusions OSA exacerbates airway inflammation in COPD patients. CPAP treatment can improve nocturnal hypoxemia and decrease airway inflammation. [ABSTRACT FROM AUTHOR]

Prostaglandin E 2 (PGE 2) is an inflammatory mediator involved in the pathogenesis of several chronic inflammatory conditions, including endometritis. Previous studies have shown that PGE 2 accumulates in Escherichia coli -challenged ex vivo endometrial explants, increasing the expression of pro-inflammatory factors and aggravating tissue damage; these alterations are linked to key enzymes involved in the synthesis of PGE 2 , including cyclooxygenases-2 (COX-2) and microsomal PGES-1 (mPGES-1). In this study, we aimed to investigate whether administration of PGE 2 modulated the activities of nitric oxide synthase 2 (NOS2), platelet-activating factor receptor (PAFR), and matrix metalloproteinase (MMP)-2 in E. coli- challenged ex vivo bovine endometrial explants. Our findings showed that COX-2 and mPGES-1 inhibitors significantly reduced NOS2, PAFR, and MMP-2 expression in the E. coli -challenged ex vivo endometrial explants. In addition, NOS2, PAFR, and MMP-2 expression levels were strongly increased in response to treatment with 15-prostaglandin dehydrogenase inhibitors in the E. coli- challenged ex vivo endometrial explants. However, these stimulatory effects could be blocked by PGE 2 receptor 4 (EP4) and protein kinase A (PKA) inhibitors. Overall, these findings show that pathogenic PGE 2 upregulated NOS2, PAFR, and MMP-2 expression, which may enhance inflammatory damage via the EP4/PKA signaling pathway in E. coli- challenged ex vivo endometrial explants. • Pathogenic bacteria (E. coli) infected bovine endometrial tissue in vitro. • PGE 2 promotes NOS2, PAFR, and MMP-2 expression in E. coli -infected bovine endometrial tissues in vitro. • PGE 2 promotes NOS2, PAFR, and MMP-2 expression via the prostaglandin E 2 receptor 4/protein kinase A signaling pathway. [ABSTRACT FROM AUTHOR]

• NLRP3 engaged in the secretion of inflammatory mediators after E. coli treatment. • NLRP3 engaged in the activation of MAPK and NF-κB signaling-pathway. • NLRP3 engaged in caspase1 signaling-pathway activation after E. coli treatment. • NLRP3 contributes to liver damage in mice after E. coli infection. The host Toll-like Receptor-2 (TLR2) and Toll-like Receptor-4 (TLR4) play critical roles in defense against Escherichia coli (E. coli) infection is well-known. The NLR pyrin domain-containing 3 (NLRP3) inflammasome is also an important candidate during the host-recognized pathogen, while the roles of NLRP3 in the host inflammatory response to E. coli infection remains unclear. This study aimed to explore the roles of NLRP3 in regulating the inflammatory response in E. coli infection-induced mice. Our result indicated that compared to wild-type mice, the TLR2-deficient (TLR2-/-), TLR4-deficient (TLR4-/-), and NLRP3-deficient (NLRP3-/-) mice had significant decrease in liver damage after stimulation with Lipopolysaccharide (LPS, 1 μg/mL), Braun lipoprotein (BLP, 1 μg/mL), or infected by WT E. coli (1 × 107 CFU, MOI 5:1). Meanwhile, compared with wild-type mice, the TNF-α and IL-1β production in serum decreased in TLR2-/-, TLR4-/-, and NLRP3-/- mice after LPS, BLP treatment, or WT E. coli infection. In macrophages from NLRP3-/- mice showed significantly reduced secretion of TNF-α and IL-1β in response to stimulation with LPS, BLP, or WT E. coli infection compared with macrophages from wild-type mice. These results indicate that besides TLR2 and TLR4, NLRP3 also plays a critical role in host inflammatory responses to defense against E. coli infection, and might provide a therapeutic target in combating disease with bacterium infection. [ABSTRACT FROM AUTHOR]