IL-33 Mediated Inflammation in Chronic Respiratory Diseases —Understanding the Role of the Member of IL-1 Superfamily

Conclusion Analysis of the pleiotropic effects of IL-33 on multiple immunological cells (macrophages, mastocytes), as well as neurological cells of medulla oblongata, dorsal root ganglion, antigen-induced arthritis system, carrageen, and formalin, shows that this alarmin plays curtail, yet not fully known role in mediating inflammation, especially in chronic inflammatory pulmonary diseases such as asthma, COPD, and OSA. Taken into consideration the engagement in this process, in particular of mastocytes and their secretion of CXCL2, 4, 8, and other cytokines, there is no doubt regarding the etiopathogenic role of IL-33 in the development of asthma in response to various stimuli damaging bronchial epithelial cells. Additionally, IL-33 intensifies recruitment of eosinophils, macrophages, and Th2 lymphocytes, which again confirms its inflammatory role. Particularly important in the context of aggravation of chronic inflammation and progression of respiratory disease is IL-33 mediated influx of neutrophils and macrophages. As these cells secrete IL-1β, TNF-α, and release proteases (elastases, metalloproteinases, cathepsins, and proteinases), it is only a logical consequence that IL-33 is involved in development of lung emphysema and chronic bronchial inflammation. It is worth mentioning that IL-33 expression is enhanced following exposure to cigarette smoke, which correlates with increased number of lymphocytes CD8+, resulting in the release of perforin and g...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research