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Background: Psoriasis is an autoimmune disease that is chronic, inflammatory, and caused by T cells. It affects the skin, nails, mucous membranes, and joints, yet not the hair. It affects about 2–3% of people worldwide, equally divided between the sexes. It affects people from 1 to 18 years old. Objective: The objective was to assess the serum level of IL-5 and establish a relationship between it and the severity of psoriasis vulgaris in patients with mild, moderate, and severe cases. Materials and Methods: This case–control study was conducted over the course of six months, from November 2020 to April 2021 at the Beni-Suef University Hospital’s outpatient clinic for dermatology, venereology, and andrology. Fifty patients with varying degrees of psoriasis vulgaris and forty age- and sex-matched, seemingly healthy controls were included in the study. A physical examination, history, and family history were all taken into consideration for the diagnosis, which was also supported by a thorough cutaneous examination of every case. The Psoriasis Area Severity Index (PASI) score was used to grade them. Furthermore, 5 mL of blood was taken out for testing. Studies pertaining to IL-5. Results: IL-5 levels were noticeably higher in the PV group than in the control group. Conclusion: The current study may add to our understanding and provide some insight into the potential involvement of IL-5 in the pathophysiology of psoriasis. Biologic treatments against IL-5 may be useful in the treatment of psoriasis. [ABSTRACT FROM AUTHOR]

Objective: To evaluate eosinophil peroxidase (EPX) as a biomarker for tissue levels of eosinophilia, cytokines, and chemokines within chronic rhinosinusitis (CRS). Methods: Twenty‐eight subjects undergoing sinonasal surgery were prospectively enrolled. Ethmoid tissue was analyzed with an in‐house EPX immunoassay and a 48‐plex cytokine‐chemokine array. Clinical severity was assessed using SNOT‐22 and Lund‐Mackay scores. Subjects were grouped as follows: controls, polyp status (CRS with [CRSwNP] and without nasal polyps [CRSsNP]), tissue eosinophilia (eosinophilic CRS [eCRS], non‐eosinophilic CRS [neCRS]), or combinations thereof (eCRSwNP, eCRSsNP, neCRSsNP). eCRS was defined as >10 eosinophils per high power field (HPF). Subjects without CRS or asthma were enrolled as controls. Results: EPX was elevated in CRSwNP compared to control (p = 0.007), in eCRS compared to neCRS (p = 0.002), and in eCRSwNP along with eCRSsNP compared to neCRSsNP (p = 0.023, p = 0.015, respectively). eCRS displayed elevated IL‐5 compared to neCRS (p = 0.005). No significant differences in EPX or IL‐5 were observed between eCRSwNP and eCRSsNP. IL‐5 was elevated in eCRSwNP (p = 0.019) compared neCRSsNP. Area under the receiver operator characteristic curve was 0.938 (95% CI, 0.835–1.00) for EPX and tissue eosinophilia, with an optimal cut‐point of 470 ng/mL being 100% specific and 81.25% sensitive for tissue eosinophilia. Linear regression revealed a strong correlation between EPX and IL‐5 (R2 = 0.64, p < 0.001). Comparing EPX and IL‐5, only EPX displayed significant correlation with SNOT‐22 (p = 0.04) and Lund‐Mackay score (p = 0.004). Conclusion: EPX is associated with tissue eosinophilia in CRS patients regardless of polyp status. EPX correlates with IL‐5 and could be potentially considered a biomarker for anti‐IL‐5 therapies. Level of Evidence: 3 Laryngoscope, 134:69–78, 2024 [ABSTRACT FROM AUTHOR]

Introduction: Mepolizumab is a treatment option in patients with severe eosinophilic asthma, which inhibits interleukin-5. The aim of this study was to evaluate the clinical features and laboratory data of patients with severe eosinophilic asthma who were classified as super-responders, partial responders, or nonresponders to mepolizumab treatment. Methods: In this retrospective real-life study, the clinical features and laboratory data were compared between groups of patients with severe eosinophilic asthma who were classified as super-responders, partial responders, or nonresponders to mepolizumab treatment. Results: Evaluation was made of a total of 55 patients, comprising 17 (30.9%) males and 38 (69.1%) females with a mean age of 51.28 ± 14.32 years. All the patients were receiving mepolizumab treatment for severe eosinophilic asthma, with 17 (30.9%) patients evaluated as super-responders, 26 (47.3%) as partial responders, and 12 (21.8%) as nonresponders. After mepolizumab treatment, there was a statistically significant decrease in asthma exacerbations, the number of oral corticosteroids (OCSs) used, the rate of hospitalization due to asthma attacks, and the eosinophil count (cells/µL) (p < 0.001, p < 0.001, p < 0.001, and <0.001, respectively). A statistically significant increase was determined in the forced expiratory volume in 1 s (FEV1) value (p = 0.010) and asthma control test (ACT) score (p < 0.001) after mepolizumab treatment. The baseline eosinophil count, eosinophil/lymphocyte ratio and FEV1 (%) values were significantly higher in the super-responder and partial responder groups (p < 0.001, p = 0.002, and p = 0.002, respectively). The baseline ACT score and the rate of chronic sinusitis with nasal polyps were significantly higher in the partial responder group (p = 0.004, p = 0.015, respectively). The rate of regular OCS use before mepolizumab treatment was significantly higher in the nonresponder group (p = 0.049). As a result of the receiver operating characteristics curve analysis, the blood eosinophil count (area under the curve [AUC]: 0.967, p < 0.001), eosinophil/lymphocyte ratio (AUC: 0.921, p < 0.001), and FEV1 (%) (AUC: 0.828, p = 0.002) were found to have diagnostic value in predicting the response to mepolizumab treatment in patients with severe eosinophilic asthma. Conclusion: Baseline eosinophil count, eosinophil/lymphocyte ratio, and FEV1 (%) were found to be important predictors of response to mepolizumab treatment. Further studies are needed to define the characterization of mepolizumab responders in the real world. [ABSTRACT FROM AUTHOR]

Aims Group 2 innate lymphoid cells (ILC2s) regulate adaptive and innate immunities. In mouse heart, production of myocardial infarction (MI) increased ILC2 accumulation, suggesting a role for ILC2 in cardiac dysfunction post-MI. Methods and results We produced MI in ILC2-deficeint Rorafl/flIl7rCre/+ mice and in Icosfl-DTR-fl/+Cd4Cre/+ mice that allowed diphtheria toxin-induced ILC2 depletion. Genetic or induced deficiency of ILC2 in mice exacerbated cardiac dysfunction post-MI injury along with increased myocardial accumulation of neutrophils, CD11b+Ly6Chi monocytes, and CD4+ T cells but deficiency of eosinophils (EOS) and dendritic cells (DC). Post-MI hearts from genetic and induced ILC2-deficient mice contained many more apoptotic cells than those of control mice, and Rorafl/flIl7rCre/+ mice showed thinner and larger infarcts and more collagen-I depositions than the Il7rCre/+ mice only at early time points post-MI. Mechanistic studies revealed elevated blood IL5 in Il7rCre/+ mice at 1, 7, and 28 days post-MI. Such increase was blunted in Rorafl/flIl7rCre/+ mice. Administration of recombinant IL5 reversed EOS losses in Rorafl/flIl7rCre/+ mice, but IL5 did not correct the DC loss in these mice. Adoptive transfer of ILC2, EOS, or DC from wild-type mice, but not ILC2 from Il5−/− mice improved post-MI cardiac functions in Rorafl/flIl7rCre/+ recipient mice. EOS are known to protect cardiomyocytes from apoptosis. Here we showed that DC acted like EOS in blocking cardiomyocyte apoptosis. Yet, ILC2 or IL5 alone did not directly affect cardiomyocyte apoptosis or TGF-β (transforming growth factor-β)-induced cardiac fibroblast Smad signalling. Conclusion This study revealed an indirect cardiac reparative role of ILC2 in post-MI hearts via the IL5, EOS, and DC mechanism. [ABSTRACT FROM AUTHOR]

Ankylosing spondylitis (AS) is an inflammatory disease that belongs to the spondyloarthritis family. IL-5 and IL-9 belong to the group of Th2 cytokines of anti-inflammatory nature. Polymorphisms in their coding genes have been so far associated with various inflammatory diseases, but there are no reports regarding their involvement in AS pathogenesis to date. The purpose of the study was to investigate relationships between IL5 and IL9 genetic variants with AS susceptibility, clinical parameters as well as response to therapy with TNF inhibitors. In total 170 patients receiving anti-TNF therapy and 218 healthy controls were enrolled in the study. The genotyping of IL5 rs2069812 (A > G) and IL9 rs2069885 (G > A) single nucleotide polymorphisms was performed using the Real-Time PCR method based on LightSNiP kits assays. The present study demonstrated significant relationships between IL5 rs2069812 and IL9 rs2069885 polymorphisms and response to anti-TNF therapy. Presence of the IL5 rs2069812 A allele in patients positively correlated with better response to treatment (p = 0.022). With regard to IL9 rs2069885, patients carrying the A allele displayed better outcomes in anti-TNF therapy (p = 0.046). In addition, IL5 rs2069812 A and IL9 rs2069885 A alleles were associated with lower CRP and VAS values. The obtained results may indicate a significant role for IL-5 and IL-9 in the course of AS and response to anti-TNF therapy. [ABSTRACT FROM AUTHOR]

Eosinophilic disorders include a wide array of conditions in which eosinophils play a primary pathophysiologic role. While historically treated with corticosteroids and immunosuppressants, knowledge of eosinophil biology has led to the development of several biologics targeting eosinophils. In this review, we discuss the current US Food and Drug Administration (FDA) approved eosinophil-specific biologics targeting IL-5 (mepolizumab and reslizumab) and IL-5R (benralizumab) along with biologics under investigation targeting siglec-8 (lirentelimab). We discuss efficacy and safety data from trials of these medications in conditions including eosinophilic asthma, hypereosinophilic syndrome (HES), eosinophilic granulomatosis with polyangiitis (EGPA), chronic rhinosinusitis with nasal polyposis (CRSwNP), eosinophilic esophagitis (EoE), and eosinophilic gastrointestinal disease (EGID). Additionally, we discuss case reports utilizing these medications in conditions including drug reaction with eosinophilia and systemic symptoms (DRESS), allergic bronchopulmonary aspergillosis (ABPA), and eosinophilic pneumonia, among others. While eosinophilic targeting biologic therapy has been successful in eosinophilic asthma, HES, EGPA, and CRSwNP leading to FDA approval for these conditions, trials treating EoE and EGID have been disappointing to date. Given the increasing number of trials utilizing these biologics, it will be imperative for the allergist-immunologist to stay up to date on the latest treatment options to provide the most optimal care for eosinophilic disorders.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by nasal obstruction, reduced sense of smell, rhinorrhea, and facial pain for more than 12 weeks, significantly affecting quality of life (QoL), especially in patients with NSAID-exacerbated respiratory disease (NERD). Initial treatment includes intranasal corticosteroids and nasal irrigations, followed by systemic corticosteroids (SC) in severe cases, as well as endoscopic sinus surgery (ESS) and biological agents. Mepolizumab, a monoclonal antibody against IL-5, has been shown to reduce eosinophilic inflammation in CRSwNP. This study evaluates the improvement in quality of life of patients with CRSwNP treated with mepolizumab before December 2023, recorded by the RINOSUR group. A retrospective observational multicenter cohort study is presented in adult patients with severe asthma and concomitant CRSwNP, treated with mepolizumab 100 mg. Variables such as sex, asthma, allergies, NERD, corticosteroid dependence, and serum eosinophil count were recorded. All patients underwent nasal endoscopy and completed the SNOT22 questionnaire. Therapeutic response was evaluated at 12 months. Out of 143 patients recruited, only 28.6% had the necessary data. 61% were women with a mean age of 55 years. All were corticosteroid-dependent and had required at least one ESS. A 22% reduction in SC cycles was observed, and no patient required revision surgery in the 12 months following treatment. The SNOT22 score was reduced by 53 points, and serum eosinophilia also showed a significant decrease. Mepolizumab is effective in treating severe uncontrolled CRSwNP, improving QoL and reducing dependence on systemic corticosteroids. Its activity is monitored by peripheral blood eosinophilia. Consistency in data collection is crucial to evaluate efficacy and manage the disease., (Copyright © 2024 Sociedad Española de Otorrinolaringología y Cirugía de Cabeza y Cuello. Published by Elsevier España, S.L.U. All rights reserved.)

Background: There is no trial to make a diagnostic tool of allergic rhinitis (AR) utilizing biomarkers from nasal fluid. Base on previous studies, we selected following five biomarkers in nasal fluids that represent the characteristics of allergic reactions: tryptase, eosinophil cationic protein (ECP), interleukin 5 (IL-5), Clara cell protein 16 (CC16) and CC16-to-albumin ratio. Objective: This study aimed to identify biomarkers in nasal discharge that may be used in biosensors to diagnose AR as an additional diagnostic tool. Methods: Patients showed rhinorrhea and tested positive on allergic skin and specific immunoglobulin E (IgE) tests were included in the AR group. The non-AR group included individuals no dominant nasal symptoms and tested negative on allergy tests. Nasal lavage fluid samples were collected from all participants. Biomarkers in the samples were quantified using enzyme-linked immunosorbent assay. Results: Forty-five patients with AR and 28 non-AR subjects were enrolled in this study. Comparing the concentrations of biomarkers, the concentrations of tryptase and IL-5 were significantly higher in the AR group than in the NAR group. And CC16 level and CC16-to-albumin ratio were significantly lower in the AR group. In the combination of tryptase or CC16-to-albumin ratio, the sensitivity was 90.7% and the specificity was 64.3% (p = 0.013). Conclusion: The combination of "tryptase or CC16-to-albumin" could be used as a screening tool for AR. Although this diagnostic method could not replace conventional diagnostic tools, we could consider the method we proposed as an additional screening tool for patients who could not undergo allergy tests. [ABSTRACT FROM AUTHOR]

Objective: Interleukin-5 (IL-5) is a cytokine known to play major role in the regulation of eosinophil formation, maturation, recruitment, and survival. Hence, an increased production of IL-5 may be contributed to the pathogenesis of eosinophil-dependent inflammatory diseases such as asthma. Methods: A total of 85 children, including 59 males and 26 females with asthma with ages between 1 year and 16 years, attended the Respiratory Clinic at Karbala pediatric hospital, with a nonasthmatic children group which have the same age and gender. Restriction fragment length polymerase chain reaction was performed to determine IL-5 C-703T genetic polymorphisms. Total immunoglobulin E (IgE) level was measured using the EUROIMMUN IgE ELISA kit and serum IL-5 levels using Elabscience ELISA kit. The absolute eosinophil count was measured by five differential automated hematology analyzers and confirmed by the examination of peripheral blood smear. Results: The TT genotype of IL-5 C-703T polymorphism was associated with asthmatic children (P: 0.033). In addition, TT genotype was associated with increase of serum IL-5 levels and high absolute eosinophil count (P = 0.008 and 0.021, respectively). Whereas, CT genotype of IL-5 C-703T was found to be associated with high total serum IgE (P < 0.001). Conclusions: Asthma in children is associated with IL-5 C-703T polymorphism. In addition, IL-5 C-703T polymorphism has impact on IL-5 levels and eosinophil count. TT genotype of IL-5 C703T consider a risk factor for mild asthma in Iraqi asthmatic children.

Background: Interleukin-5 (IL-5) is a cytokine associated with the cause of several allergic diseases such as asthma due to their function in growth, activation, and maturation of eosinophils and stimulates B-cell growth and increases immunoglobulin E (IgE) secretion. The study aims to measure the IL-5 level in asthmatic children and detect the relationship between IL-5 level with eosinophils, total serum IgE level, and asthma severity. Methods: Eighty asthmatic children, including 55 males and 25 females with asthma who aged between 1 and 16 years collected at Kerbala Teaching Hospital for Children, were measured IL-5 level using Elabscience ELISA kit and measured total IgE level using EUROIMMUN IgE ELISA kit. However, absolute eosinophils count was examined by peripheral blood smear. In addition, the clinical characteristics of the patients were recorded by a questionnaire. Results: There was a significant difference in IL-5 level in asthma patients depending on sex, absolute eosinophil count, and use of treatment (P = 0.046, 0.046, and 0.001, respectively). However, there was no effect on the IL-5 level at asthmatic children depending on the age, body mass index, resident, exposure to cigarette smoking, family history of asthma/allergic diseases, asthma severity, and total serum IgE (P = 0.936, 0.769, 0.154, 0.898, 0.614, 0.550, and 0.874, respectively). Conclusions: IL-5 level had a positive correlation with absolute eosinophils count but not with total serum IgE. In addition, IL-5 level was a poor indicator of asthma severity.

The review discusses the problems associated with the treatment of patients with severe resistant to therapy asthma: prevalence, socio-economic burden, impact on quality of life. The phenotype of bronchial asthma with eosinophilic inflammation, frequency of occurrence, clinical features, and modern approaches to therapy are discussed in detail, including the use of a drug of monoclonal antibodies against interleukin 5-reslizumab.

Abstract Bronchial asthma (BA) is a chronic inflammatory disease with a marked heterogeneity in pathophysiology and etiology. The heterogeneity of BA may be related to the inducing mechanism(s) (allergic vs non-allergic), the histopathological background (eosinophilic vs non-eosinophilic), and the clinical manifestations, particularly in terms of severity and frequency of exacerbations. Asthma can be divided into at least two different endotypes based on the degree of Th2 inflammation (T2 ‘high’ and T2 ‘low’). For patients with severe uncontrolled asthma, monoclonal antibodies (mAbs) against immunoglobulin E (IgE) or interleukin (IL)-5 are now available as add-on treatments. Treatment decisions for individual patients should consider the biological background in terms of the “driving mechanisms” of inflammation as this should predict the patients’ likely responses to treatment. The question is not whether an anti-IgE or an anti-eosinophilic strategy is more effective, but rather what the mechanism is at the origin of the airway. While IgE is involved early in the inflammatory cascade and can be considered as a cause of allergic asthma, eosinophilia can be considered a consequence of the whole process. This article discusses the different roles of the IgE and IL-5/eosinophil pathways in the pathogenic mechanisms of airway inflammation occurring in allergic asthma, and the possible reasons to choose an anti-IgE mAb or anti-IL-5 treatment.

Subclinical inflammatory reaction is associated with non-insulin dependent diabetes. therefore, the aim of the present study is to describe the effect of the three cytokines: interferon γ (iFN-γ), interleukin (IL)-4 and IL-5 on the development of type 2 diabetes (T2D). Forty-five volunteers (after their permission) were participated in this work; according to their clinical examination and laboratory investigations (fasting blood sugar, 2 hours postprandial, HbA1C and lipid profile), they were divided into thirteen control (non-diabetic) (five females and eight males) and thirty-two diabetic patients (twenty- one females and eleven males). thereafter, their sera were evaluated for C-reactive protein (CRP), IFN-γ, Il-4 and Il-5. the results revealed an increasing trend of CRP and a significant increase of iFN-γ in diabetic patients with no sex difference. a positive correlation between iFN-γ and both IL-4 and IL-5 in control, and a positive correlation between IL-4 and IL-5 in diabetic patients had been visualized. these results denoted that there may be an association of the pro-inflammatory cytokines in the etiology of diabetes mellitus type 2. [ABSTRACT FROM AUTHOR]

The choice of biological drug that would be optimal for the patient is determined by many factors. The authors tried to summarize the current knowledge about biological drugs used in the treatment of severe persistent asthma. Fortunately, one of the most important factors, ie reimbursement of the drug from public health insurance funds and a possible supplement to the patient in the conditions of the Czech Republic, does not play a more fundamental role, as the relevant products are covered by almost all public funds. The authors discuss the pharmacokinetic properties of drugs, their dosage, route of administration, adherence and patient preferences. [ABSTRACT FROM AUTHOR]

Asthma is a chronic inflammation of the respiratory tract characterized by coughing, shortness of breath, wheezing and limited expiratory airflow. Interleukin 10 (IL-10) is a cytokine produced by T regulators which functions to suppress pro-inflammatory production and development. Interleukin 5 (IL-5) is glycoprotein produced by Th2 which acts as a proinflammatory agent. This study aimed to analyze how to balance between IL-10 and IL-5 levels on persistent atopic asthma. The study design was an experimental research method with invitro study used isolation and cell culture of Peripheral Blood Mononuclear Cell (PBMC) with negative control Roswell Park Memorial Institute (RPMI) medium, positive control Phytohaemaglutinin (PHA) and house dust mite allergen stimulation 10 µl. This study involved 39 samples asthmatic. There was a significant increase in IL-5 levels after stimulation of house dust mite allergens with p: 0.000; there was a significant decrease in IL-10 levels after house dust mite allergen stimulation with p: 0.000. Our study suggests that IL-5 and IL-10 balance is related to persistent atopic asthma after house dust mite allergen Der p stimulation. [ABSTRACT FROM AUTHOR]

Background: Invasive and costly endoscopic diagnosis is obligatory for the diagnosis and monitoring of eosinophilic esophagitis (EoE). This study aims to evaluate the usefulness of serum biomarkers involved in eosinophil-mediated inflammation in the management of EoE. Methods: A prospective cohort study was conducted in 58 patients with dysphagia. Each participant completed a health questionnaire, underwent esophagogastroduodenoscopy with esophageal biopsy for histopathological examination and assessment of total, inflammatory and fibrostenotic Eosinophilic Esophagitis Reference Score (EREFS). Serum levels of interleukin 5 (IL-5), interleukin 13 (IL-13), transforming growth factor β1 (TGF-β1), major basic protein (MBP), and eotaxin 3 were determined by enzyme immunoassays. Total of 16 patients meeting the histological criteria for EoE were treated with proton pump inhibitors for 8 weeks, and then the same diagnostics was performed again. Results: Statistically significantly higher concentrations of MBP and TGF-β1 were demonstrated in the group of patients with EoE, while MBP and eotaxin 3 correlated with the peak eosinophil count (PEC). Baseline MBP levels and eotaxin 3 after treatment significantly positively correlated with EREFS. There was a negative correlation between IL-13 and fibrostenotic EREFS. Additionally, after treatment, a negative correlation TGF-β1 was noted with the inflammatory EREFS and a positive correlation with the fibrostenotic EREFS. Conclusions: The potential role of MBP in predicting the diagnosis of EoE, eotaxin 3 in predicting the advancement and correlation of IL-13 and TGF-β1 in differentiating the inflammatory and fibrotic course of the disease may facilitate the management and individualization of EoE therapy.

Improved knowledge about the pathogenesis of asthma has facilitated the development of novel drugs and provided hope for patients with severe asthma. After the short- and long-term success of omalizumab in severe allergic phenotype, researchers have targeted patients with severe eosinophilic asthma who comprise up to 45% of adult severe asthma. Interleukin (IL)-5 and IL-5 receptor subunit α play crucial roles in the development, maturation, and operation of eosinophils. Currently, patients treated with anti-IL-5 biologicals depleting eosinophils experience the positive efficacy of these drugs, especially with regard to the reduction of exacerbation rate. The aim of this review was to shed light on severe eosinophilic asthma treatment with these new currently available agents selectively targeting IL-5 or its receptor, discussing their usage including pre-treatment concerns, such as selecting the target population and choosing the right agent among them, and subsequent assessment of relevant effect and safety issues. [ABSTRACT FROM AUTHOR]

Resumen INTRODUCCIÓN La rinosinusitis crónica es la inflamación de la mucosa nasosinusal de duración superior a 12 semanas. Se distinguen dos formas clínicas: rinosinusitis crónica con pólipos y sin pólipos. Los pacientes con rinosinusitis crónica con pólipos presentan niveles elevados de interleukina 5, la cual promueve la diferenciación y supervivencia de eosinófilos, por lo que se ha propuesto minimizar su circulación como una nueva estrategia de tratamiento. Sin embargo, no hay claridad respecto a su real efectividad. MÉTODOS Para responder esta pregunta utilizamos Epistemonikos, la mayor base de datos de revisiones sistemáticas en salud, la cual es mantenida mediante búsquedas en múltiples fuentes de información, incluyendo MEDLINE, EMBASE, Cochrane, entre otras. Extrajimos los datos desde las revisiones identificadas, reanalizamos los datos de los estudios primarios, realizamos un metanálisis y preparamos una tabla de resumen de los resultados utilizando el método GRADE. RESULTADOS Y CONCLUSIONES Identificamos tres revisiones sistemáticas que en conjunto incluyeron tres estudios primarios, todos correspondientes a ensayos aleatorizados. Concluimos que los inhibidores de interleukina 5 podrían disminuir el puntaje de pólipos nasales. Si bien podrían asociarse a efectos adversos, estos serían poco frecuentes y de baja severidad. Sin embargo, la certeza de la evidencia es baja.

Asthma is a common chronic inflammatory disease in which lung airways narrow and produce extra mucus. Numerous medications, such as steroids, are used to prevent or control asthmatic symptoms, but side effects are associated with those medications. There are reports of anti-inflammatory, antibacterial, and antiparasitic effects of terpene, a volatile organic compound (VOC) in conifers. VOCs easily enter a gaseous form, and wood products are good sources of VOCs. However, only a few studies have been conducted on the effect on asthma of VOCs emitted by wood. In this study, we examined the effects of VOCs diffused from wood panels on ovoalbumin (OVA)-induced asthma in a mouse model. The mice were intraperitoneally sensitized with 10 μg of OVA with aluminum hydroxide on days 0, 7, and 14. From day 21 to day 26, the mice were challenged with 2% OVA intranasally for 30 min. For VOC treatment, asthma model mice were placed in polyacrylamide chambers containing wood panels of Chamaecyparis obtusa, Pinus densiflora, Pinus koraiensis, or Larix kaempferi. On day 27, serum, lung tissue, and bronchoalveolar lavage fluids were prepared for H&E staining, qRT-PCR, ELISA, and Diff-Quik staining, as appropriate. OVA treatment induced hypertrophy of the bronchiolar wall. The budesonide group and all four of the wood panel-exposed groups showed less thickening of the bronchiolar wall and downregulated transcriptional expressions of cytokines such as interleukin-4 (IL-4) and interleukin-13 (IL-13). The serum tumor necrosis factor-α (TNF-α) mRNA expression level was significantly decreased only in the C. obtusa group, but the serum IL-4 levels were decreased in all wood panel treatment groups. Diff-Quik staining of bronchoalveolar lavage fluids revealed a decrease in the number of granulocytes in all wood panel treatment groups. The results suggest that VOCs from C. obtusa, P. densiflora, P. koraiensis and L. kaempferi produce antiasthmatic effects by regulating the production of IL-4, IL-9, IL-13, TNF-α. [ABSTRACT FROM AUTHOR]

Eosinophilic esophagitis (EoE) is a disorder that has been identified recently, thus knowledge about it, its pathogenesis, and potential etiologies has spread in an era where the medical community and the public are receiving the information and discussing it as it appears in the medical literature. Because physiology, pathology, and pathophysiology are difficult to explain in layman terms, the author has used photographs taken in remote areas of the Amazon to create visual similes within a narrative that brings the scientific and medical concepts of the knowledge on EoE to a level that allows both medical and non-medical persons to grasp and discuss their significance. This set of photographs when presented to audiences has generated interest in the disorder as well as in the Amazon and its natural flora and fauna. The author hopes that this pictorial introduction sets the stage for the multiple novel topics reviewed and presented in this issue. [ABSTRACT FROM AUTHOR]

Inhibiting the interleukin 17 pathway is of interest in a number of autoimmune diseases. Herein, 42 fused pyrimidines have been evaluated as interleukin 17 secretion inhibitors using a phenotypic assay with peripheral blood mononuclear cells. 7 H -Pyrrolo [2,3- d ]pyrimidin-4-amines having aryl groups at C-5 or C-6 were found more active than the corresponding thieno- and furopyrimidines. Low cytotoxicity was seen for the most active inhibitors. However, the pyrrolopyrimidines also inhibit interleukin 5 secretion, suggesting that selective interleukin 17 inhibitors should rather be based on furopyrimidines. Profiling towards a panel of 51 kinases and assays towards the retinoic acid receptor-related orphan receptor gamma were performed in order to identify the compounds mode of action. [ABSTRACT FROM AUTHOR]

Objective Obesity is a metabolic disorder that has reached epidemic proportions worldwide and leads to increased risk for diabetes, cardiovascular disease, asthma, certain cancers, and various other diseases. Obesity and its comorbidities are associated with impaired adipose tissue (AT) function. In the last decade, eosinophils have been identified as regulators of proper AT function. Our study aimed to determine whether normalizing the number of AT eosinophils in obese mice, to those of lean healthy mice, would reduce obesity and/or improve metabolic fitness. Methods C57BL/6J mice fed a high fat diet (HFD) were simultaneously given recombinant interleukin-5 (rIL5) for 8 weeks to increase AT eosinophils. Metabolic fitness was tested by evaluating weight gain, AT inflammation, glucose, lipid, and mixed-meal tolerance, AT insulin signaling, energy substrate utilization, energy expenditure, and white AT beiging capacity. Results Eosinophils were increased ∼3-fold in AT of obese HFD-fed mice treated with rIL5, and thus were restored to levels observed in lean healthy mice. However, there were no significant differences in rIL5-treated mice among the above listed comprehensive set of metabolic assays, despite the increased AT eosinophils. Conclusions We have shown that restoring obese AT eosinophils to lean healthy levels is not sufficient to allow for improvement in any of a range of metabolic features otherwise impaired in obesity. Thus, the mechanisms that identified eosinophils as positive regulators of AT function, and therefore systemic health, are more complex than initially understood and will require further study to fully elucidate. [ABSTRACT FROM AUTHOR]

Background and objective: Th9 cells producing interleukin (IL) 9 are novel subset of CD4+ T helper cells, which might contribute to airway inflammation in asthma. Moreover, the effect of IL-9 on eosinophils is still not fully understood. Study aim was to evaluate peripheral blood Th9 cells and eosinophil apoptosis in allergic asthma patients. Materials and methods: Eighteen patients with allergic asthma and fourteen patients with allergic rhinitis were examined. Control group included sixteen healthy subjects. Allergic asthma and rhinitis patients did not use corticosteroids and antihistamines at least for 1 week. Peripheral blood eosinophils and CD4+ cells were isolated by high density gradient centrifugation and magnetic separation. Th9 cells and apoptotic eosinophils were estimated by flow cytometer. Serum IL-9 and IL-5 concentration were determined by ELISA. Results: Peripheral blood Th9 cells percentage was increased in allergic asthma group compared with allergic rhinitis and control group (0.74% ± 0.32% vs. 0.19% ± 0.10% and 0.15% ± 0.08%, respectively, P

The definition of asthma has changed considerably in recent years, to the extent that asthma is no longer considered a single disease but a heterogeneous disorder that includes several phenotypes and, possibly, endotypes. A more detailed analysis of the immunological mechanisms underlying the pathogenesis of asthma shows interleukin 5 (IL-5) to be a crucial cytokine in several asthma phenotypes. In fact, IL-5 exerts selective action on eosinophils, which, in turn, sustain airway inflammation and worsen asthma symptoms and control. Clinical trials have shown drugs targeting IL-5 or its receptor alpha subunit (IL-5Ra) to be a promising therapeutic approach to severe asthma, whose characteristics render standard therapy of little use: systemic corticosteroids only partially control the disease and have well-known adverse effects, and omalizumab is used for allergic subtypes. Analysis of the design process of clinical trials reveals the importance of patient selection, taking into account both clinical data (e.g., exacerbations, lung function, and quality of life) and biomarkers (e.g., eosinophils, which are predictive of therapeutic response).

Background Familial eosinophilia ( FE) is a rare autosomal dominant inherited disorder characterized by the presence of lifelong peripheral eosinophilia (>1500/μL). Mapped to chromosome 5q31-q33, the genetic cause of FE is unknown, and prior studies have failed to demonstrate a primary abnormality in the eosinophil lineage. Objective The aim of this study was to identify the cells driving the eosinophilia in FE. Methods Microarray analysis and real-time PCR were used to examine transcriptional differences in peripheral blood mononuclear cells ( PBMC), and in purified cell subsets from affected and unaffected family members belonging to a single large kindred. Cytokine levels in serum and PBMC culture supernatants were assessed by suspension array multiplexed immunoassays. Results Whereas IL-5 m RNA expression was significantly increased in freshly isolated PBMC from affected family members, this was not accompanied by increased m RNA expression of other Th2 cytokines ( IL-4 or IL-13). Serum levels of IL-5 and IL-5 receptor α, but not IgE, were similarly increased in affected family members. Of note, IL-5 m RNA expression was significantly increased in purified CD3+ CD4+, CD14+, CD19+, and ILC2 cells from affected family members, as were IL-5 protein levels in supernatants from both stimulated PBMC and ILC2 cultures. Conclusions These data are consistent with the hypothesis that the eosinophilia in FE is secondary to dysregulation of IL-5 production in PBMC (and their component subsets). [ABSTRACT FROM AUTHOR]

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