Toll-Like Receptor-4-Mediated Inflammation is Involved in Intermittent Hypoxia-Induced Lung Injury
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INTERMITTENT HYPOXIA-INDUCED LUNG INJURY
Toll‑Like Receptor‑4‑Mediated Inflammation is Involved in Intermittent Hypoxia‑Induced Lung Injury Fangfang Zou1 · Xiaoli Su2 · Pinhua Pan2 Received: 26 February 2020 / Accepted: 31 July 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose Intermittent hypoxia (IH) is a recognized risk factor for multiple organs damage, resulting in lung injury. Its pathophysiology is still poorly understood. Toll-like receptor 4 (TLR4) signaling plays a critical role in host immune response to invading pathogen and non-infectious tissue injury. The role of TLR4-mediated inflammation in IH-induced lung injury was investigated in this study. Methods Lean adult male TLR4-deficient ( TLR4−/−) mice and their controls (C57BL/6 mice) were exposed to either IH (FiO2 6–8% for 25 s, 150 s/cycle, 8 h/day) or air (normoxic mice) for 6 weeks. Animals were sacrificed after 6-week exposure, and the lung tissues were harvested for morphological and inflammatory analyses. The expression of TLR4 and nuclear factor kappa-B (NF-κB) P65 were examined by real-time quantitative polymerase chain reaction and immunohistochemical method. Serum cytokine levels of interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-α) were analyzed by enzymelinked immunosorbent assay. Results IH induced morphological and inflammation changes in the lung. IH for 6 weeks induced higher expression of TLR4 (C57BL/6-N vs C57BL/6-IH, P
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