RNase L Is Involved in Liposaccharide-Induced Lung Inflammation


<jats:p>RNase L mediates interferon (IFN) function during viral infection and cell proliferation. Furthermore, the role of RNase L in the regulation of gene expression, cell apoptosis, autophagy, and innate immunity has been well established in the last decade. Tissue distribution reveals that RNase L is highly expressed in the lung and other organs. However, the physiological roles of RNase L in the lung are largely unknown. In this study, we found that polysaccharide (LPS)-induced acute lung injury (ALI) was remarkably intensified in mice deficient in RNase L compared to wild type mice under the same condition. Furthermore, we found that RNase L mediated the TLR4 signaling pathway, and regulated the expression of various pro- and anti-inflammatory genes in the lung tissue and blood. Most importantly, RNase L function in macrophages during LPS stimulation may be independent of the 2-5A system. These findings demonstrate a novel role of RNase L in the immune response via an atypical molecular mechanism.</jats:p>






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Publication Info

Wei, Ruhan, Guanmin Chen, Naseh Algehainy, Chun Zeng, Chunfang Liu, Hongli Liu, Wendy Liu, Dennis Stacey, et al. (n.d.). RNase L Is Involved in Liposaccharide-Induced Lung Inflammation. Viruses, 12(1). pp. 73–73. 10.3390/v12010073 Retrieved from https://hdl.handle.net/10161/25469.

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Ruhan Wei

Assistant Professor of Pathology

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