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E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lung.
Sci Rep
January 2025
College of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese Medicine, Nanchang, 330004, China.
Allergic airway inflammation is a universal airway disease induced by inhaling allergens. Published data show that RNF128, an E3 ligase, promotes Th2 activation in the OVA-induced asthma model. Recent advances have shown that group 2 innate lymphoid cells (ILC2s) produce the cytokines IL-5 and IL-13 to mediate type 2 immune response.
View Article and Find Full Text PDFWild-Mouse-Derived Gut Microbiome Transplantation in Laboratory Mice Partly Alleviates House-Dust-Mite-Induced Allergic Airway Inflammation.
Microorganisms
December 2024
Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, 1870 Frederiksberg, Denmark.
Laboratory mice are instrumental for preclinical research but there are serious concerns that the use of a clean standardized environment for specific-pathogen-free (SPF) mice results in poor bench-to-bedside translation due to their immature immune system. The aim of the present study was to test the importance of the gut microbiota in wild vs. SPF mice for evaluating host immune responses in a house-dust-mite-induced allergic airway inflammation model without the influence of pathogens.
View Article and Find Full Text PDFIL-4R and CXCR2 Contribute to Downregulating Neutrophil-Mediated Response in the Early Stage of Fungal Extract-Induced Allergic Airway Inflammation.
Biomedicines
November 2024
Department of Immunology, Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia.
: Airborne exogenous antigen inhalation can induce neutrophil infiltration of the airways, while eosinophils migrate to the airways in allergic airway inflammation. During a bacterial infection, Th2-associated cytokine IL-4, by binding to the IL-4 receptor (IL-4R), can suppress neutrophil recruitment to the site of inflammation. In the present study, we estimated whether the IL-4-dependent suppression of neutrophil recruitment contributed to the development of an immune response in asthma.
View Article and Find Full Text PDFTriptolide alleviates allergic airway inflammation by inhibiting group 2 innate lymphoid cell function.
Int Immunopharmacol
January 2025
State Key Laboratory for Animal Disease Control and Prevention, Key Laboratory of Animal Virology of the Ministry of Agriculture, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.
Group 2 innate lymphoid cells (ILC2s) produce the type 2 cytokines IL-5 and IL-13 and contribute to type 2 immune responses, such as allergic airway inflammation. However, specific drugs, especially traditional Chinese medicines, that target lung ILC2s have rarely been reported. Here, we demonstrate that triptolide ameliorates allergic airway inflammation by suppressing ILC2 activation.
View Article and Find Full Text PDFTargeting mitochondrial function as a potential therapeutic approach for allergic asthma.
Inflamm Res
January 2025
Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, The First Dongguan Affiliated Hospital, College of Medical Technology, Guangdong Medical University, Dongguan, 523808, China.
Allergic asthma is a chronic complex airway disease characterized by airway hyperresponsiveness, eosinophilic inflammation, excessive mucus secretion, and airway remodeling, with increasing mortality and incidence globally. The pathogenesis of allergic asthma is influenced by various factors including genetics, environment, and immune responses, making it complex and diverse. Recent studies have found that various cellular functions of mitochondria such as calcium regulation, adenosine triphosphate production, changes in redox potential, and free radical scavenging, are involved in regulating the pathogenesis of asthma.
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