Background: Exposure to sulfur dioxide (SO2) increases asthma risk. Inflammatory and immune responses are typical in asthma disease. The exact effect of SO2 on modulation of the inflammatory and immune responses in asthmatic rats remains unclear.
Objectives: Here we sought to investigate the molecular mechanisms underlying the NF-κB inflammatory pathway and the Th1/Th2 imbalance in asthmatic rats exposed to SO2.
Methods: Male Wistar rats were challenged by ovalbumin (OVA) or SO2 alone or together, and then mRNA and protein levels of some inflammatory and immune genes were measured. NF-κB nuclear translocation was analyzed. Bronchoalveolar lavage (BAL), inflammatory cell counts and histopathologic examination were performed.
Results: (1) OVA plus SO2 induced abnormal pathological changes and inflammatory responses in lung relative to exposure to OVA alone; (2) showing NF-κB nuclear translocation and activation through up-regulating IKKβ mRNA and protein expression and down-regulating IκBα expression in the presence of OVA or OVA plus SO2; (3) OVA plus SO2 significantly raised TNF-α and IL-6 levels in BALF compared with the OVA group; (4) SO2 markedly elevated IL-4 levels and decreased IFN-γ levels in BALF in the asthmatic rats, stimulating IgE generation which was closely related to inhibiting the expression of Foxp3, a specific marker of regulatory T cells.
Conclusions: SO2 affects the airway inflammatory and immune responses of the asthmatic rats and enhances the susceptibility to OVA by aggravating inflammatory responses in lungs, up-regulating pro-inflammatory cytokine expression, and causing the Th1/Th2 imbalance, which might contribute to the increased risk of asthma disease.
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http://dx.doi.org/10.1016/j.chemosphere.2014.04.065 | DOI Listing |
Adv Sci (Weinh)
January 2025
Department for Functional Materials in Medicine and Dentistry, University Hospital Würzburg, Würzburg, Germany.
Studying the molecular basis of intestinal infections caused by enteric pathogens at the tissue level is challenging, because most human intestinal infection models have limitations, and results obtained from animals may not reflect the human situation. Infections with Salmonella enterica serovar Typhimurium (STm) have different outcomes between organisms. 3D tissue modeling of primary human material provides alternatives to animal experimentation, but epithelial co-culture with immune cells remains difficult.
View Article and Find Full Text PDFClin Cosmet Investig Dermatol
January 2025
Department of Clinical Laboratory, Central Hospital of Dalian University of Technology, Dalian, 116033, People's Republic of China.
Objective: Juvenile dermatomyositis (JDM) is a complex autoimmune disease, and its pathogenesis remains poorly understood. Building upon previous research on the immunological and inflammatory aspects of JDM, this study aims to investigate the role of pyroptosis in the pathogenesis of JDM using a comprehensive bioinformatics approach.
Methods: Two microarray datasets (GSE3307 and GSE11971) were obtained from the Gene Expression Omnibus database, and a list of 62 pyroptosis-related genes was compiled.
Curr Res Food Sci
December 2024
Department of Immunology, College of Basic Medical Sciences, Jilin University, 126 Xin min Street, Changchun, 130021, China.
Inflammatory bowel disorders (IBD) can lead to severe complications like perforation, bleeding, and colon cancer, posing life-threatening risks. Murray ( Murr.), rich in polysaccharides, has been utilized in traditional diets for thousands of years.
View Article and Find Full Text PDFActa Pharm Sin B
December 2024
State Key Laboratory of Bioactive Substance and Function of Natural Medicines Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
Interleukin-1 receptor-related kinase (IRAK4) is a widely expressed serine/threonine kinase involved in the regulation of innate immunity. IRAK4 plays a pivotal role as a key kinase within the downstream signaling pathway cascades of interleukin-1 receptors (IL-1R) and Toll-like receptors (TLRs). The signaling pathways orchestrated by IRAK4 are integral to inflammatory responses, and its overexpression is implicated in the pathogenesis of inflammatory diseases, autoimmune disorders, and cancer.
View Article and Find Full Text PDFActa Pharm Sin B
December 2024
Department of Molecular and Life Science, Hanyang University, Ansan 15588, Republic of Korea.
The pathophysiology of sepsis is characterized by a systemic inflammatory response to infection; however, the cytokine blockade that targets a specific early inflammatory mediator, such as tumor necrosis factor, has shown disappointing results in clinical trials. During sepsis, excessive endotoxins are internalized into the cytoplasm of immune cells, resulting in dysregulated pyroptotic cell death, which induces the leakage of late mediator alarmins such as HMGB1 and PTX3. As late mediators of lethal sepsis, overwhelming amounts of alarmins bind to high-affinity TLR4/MD2 and low-affinity RAGE receptors, thereby amplifying inflammation during early-stage sepsis.
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