Unlabelled: Recent investigations suggest an involvement of sphingosine-1-phosphate (S1P) in the pathogenesis of allergic bronchial asthma. However, the role of S1P in the development of asthma is still controversial. Our aim was to investigate the effects of intranasal application of S1P on antigen-induced airway inflammation in a mouse model of allergic bronchial asthma.
Methodology: Male BALB/c mice were actively sensitized with ovalbumin antigen, and were repeatedly challenged with aerosolized antigen. Animals also received an intranasal administration of S1P (10-5 M, 20 µL) or its vehicle (1% methanol in sterile PBS, 20 µL) 30 min prior to each antigen challenge. Histological examinations of the lungs and determination of cell number in the bronchoalveolar lavage fluids (BALFs) were studied.
Results: The airway inflammation induced by antigen exposure was significantly augmented by the intranasal administration of S1P: the cell number in BALFs of the S1P-treated, antigen-challenged mice (S1P-Challenged, 48.9±4.8 x 10(4)/mL BALF) was significantly increased as compared with those of the vehicle-treated, antigen-challenged ones (Vehicle-Challenged, 26.3±5.7 x 10(4)/mL BALF, P<0.01).
Conclusion: In mice, the intranasal administration of S1P might aggravate the antigen-induced airway inflammation.
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http://dx.doi.org/10.2174/1874306401004010082 | DOI Listing |
Clin Rev Allergy Immunol
January 2025
Postgraduate Program in Biochemistry, Federal University of Espírito Santo (UFES), Vitória, Espírito Santo, Brazil.
Asthma is a complex disease with varied clinical manifestations resulting from the interaction between environmental and genetic factors. While chronic airway inflammation and hyperresponsiveness are central features, the etiology of asthma is multifaceted, leading to a diversity of phenotypes and endotypes. Although most research into the genetics of asthma focused on the analysis of single nucleotide polymorphisms (SNPs), studies highlight the importance of structural variations, such as copy number variations (CNVs), in the inheritance of complex characteristics, but their role has not yet been fully elucidated in asthma.
View Article and Find Full Text PDFJ Allergy Clin Immunol
January 2025
Departments of Pediatrics and Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI.
Background: Rhinoconjunctivitis phenotypes are conventionally described based on symptom severity, duration and seasonality and aeroallergen sensitization. It is not known whether these phenotypes fully reflect the patterns of symptoms seen at a population level.
Objective: To identify phenotypes of rhinoconjunctivitis based on symptom intensity and seasonality using an unbiased approach and to compare their characteristics.
Nat Commun
January 2025
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Acute and chronic inflammation are important pathologies of benign airway stenosis (BAS) fibrosis, which is a frequent complication of critically ill patients. cGAS-STING signalling has an important role in inflammation and fibrosis, yet the function of STING in BAS remains unclear. Here we demonstrate using scRNA sequencing that cGAS‒STING signalling is involved in BAS, which is accompanied by increased dsDNA, expression and activation of STING.
View Article and Find Full Text PDFJ Proteome Res
January 2025
Department of Physiology and Pathophysiology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg R3E0J9, Canada.
Annu Rev Immunol
January 2025
2Department of Medical Biochemistry and Cell Biology, University of Gothenburg, Gothenburg, Sweden; email:
The mucosal surfaces of the body are the most vulnerable points for infection because they are lined by single or multiple layers of very active epithelial cells. The main protector of these cells is the mucus system generated by the specialized goblet cells secreting its main components, the gel-forming mucins. The organization of the mucus varies from an attached mucus that is impenetrable to bacteria in the large intestine to a nonattached, more penetrable mucus in the small intestine and airways.
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