A new article titled IL-33 mediates lung inflammation by the IL-6-type cytokine Oncostatin M, published by MIRC’s Dr. Fernando Botelho and Dr. Carl Richards in the journal Mediators of Inflammation, investigates the relationship between IL-33 and Oncostatin M in lung inflammation. Th2 inflammatory responses in the lung underlie the development of a number of lung pathologies including those in allergic airway diseases. The group finds that IL-33, a cytokine induced in type II alveolar epithelial cells, plays a critical role in inducing a Th2 inflammatory response following Oncostatin M-induced inflammation.
Previously, the group established the role of Oncostatin M in inducing Th2 inflammatory responses and M2 macrophage accumulation as a mechanism towards lung inflammation. However, the role of IL-33 in the Th2 response in relation to Oncostatin M had yet to be elucidated. Dr. Botelho and Dr. Richards find that Oncostatin M-mediated M2 macrophage recruitment and Th2 cytokine production is entirely dependent on its upregulation of IL-33, which activated IL-5 and IL-13 production by ILC2 cells. Moreover, they find that IL-33 activates a positive inflammatory feedback loop, as it in turn induced the expression of Oncostatin M in macrophages. These findings lead to a better understanding of the critical mechanisms behind Th2-mediated pathologies and have broad implications for the development of therapies to treat inflammatory lung diseases.
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