The Journal of allergy and clinical immunology
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J. Allergy Clin. Immunol. · Aug 2019
Clinical TrialEpithelium-derived cystatin SN enhances eosinophil activation and infiltration through IL-5 in patients with chronic rhinosinusitis with nasal polyps.
The interaction between epithelial cells and immune cells plays an important role in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP); however, the mechanism or mechanisms underlying TH-biased inflammation in this process are largely unknown. Profiling protein expression in patients with CRSwNP by using shotgun proteomics suggested that cystatin SN (CST1), a type 2 cysteine protease inhibitor, might play a role because this was expressed with the greatest difference in patients with eosinophilic chronic rhinosinusitis with nasal polyps (ECRSwNP) and those with noneosinophilic chronic rhinosinusitis with nasal polyps (nonECRSwNP). ⋯ Epithelium-derived CST1 modulates eosinophil activation and recruitment, expression of which could be regulated by TH2 and TH17 cytokines.
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J. Allergy Clin. Immunol. · Aug 2019
Apolipoprotein E is a concentration-dependent pulmonary danger signal that activates the NLRP3 inflammasome and IL-1β secretion by bronchoalveolar fluid macrophages from asthmatic subjects.
House dust mite (HDM)-challenged Apoe-/- mice display enhanced airway hyperreactivity and mucous cell metaplasia. ⋯ APOE can function as an endogenous, concentration-dependent pulmonary danger signal that primes and activates the NLPR3 inflammasome in BALF macrophages from asthmatic subjects to secrete IL-1β. This might represent a mechanism through which APOE amplifies pulmonary inflammatory responses when concentrations in the lung are increased to greater than normal levels, which can occur during viral exacerbations of HDM-induced asthma characterized by neutrophilic airway inflammation.