Abstract
IL-33 is an alarmin that plays an integral role in lung homeostasis through its actions in wound repair, fibrosis, and remodeling processes.1 Stored in the nucleus, IL-33 is released to the cytoplasm and extracellular fluids following insult or damage that was induced by various infectious, noxious, or environmental agents.2 In addition to its role in allergic asthma,3,4 studies have demonstrated elevated IL-33 in COPD plasma,5 COPD airways,1 and idiopathic pulmonary fibrosis (IPF) lung tissues6; however, a comparative analysis of lung IL-33 expression in the setting of infectious sequalae are lacking.
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