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• W4200544093 endingPage "328" @default.
• W4200544093 startingPage "309" @default.
• W4200544093 abstract "Aspiration-induced lung injury is a common grievance encountered in the intensive care unit (ICU). It is a significant risk factor for improving ventilator-associated pneumonia (VAP) and acute respiratory distress syndrome (ARDS). Hypoxia-inducible factor (HIF)-1α is one of the primary transcription factors responsible for regulating the cellular response to changes in oxygen tension. Here, we sought to determine the role of HIF-1α and specifically the role of type 2 alveolar epithelial cells in generating the acute inflammatory response following acid and particles (CASP) aspiration. Previous studies show HIF-1 α is involved in regulating the hypoxia-stimulated expression of MCP-1 in mice and humans. The CASP was induced in C57BL/6, ODD-Luc, HIF-1α (+/+) control, and HIF-1α conditional knockout (HIF-1α (-/-) mice). Following an injury in ODD mice, explanted organs were subjected to IVIS imaging to measure the degree of hypoxia. HIF-1α expression, BAL albumin, cytokines, and histology were measured following CASP. In C57BL/6 mice, the level of HIF-1α was increased at 1 h after CASP. There were significantly increased levels of albumin and cytokines in C57BL/6 and ODD-Luc mice lungs following CASP. HIF-1α (+/+) mice given CASP demonstrated a synergistic increase in albumin leakage, increased pro-inflammatory cytokines, and worse injury. MCP-1 antibody neutralized HIF-1α (+/+) mice showed reduced granuloma formation. The NF-κB expression was increased substantially in the HIF-1α (+/+) mice following CASP compared to HIF-1α (-/-) mice. Our data collectively identify that HIF-1α upregulation of the acute inflammatory response depends on NF-κB following CASP." @default.
• W4200544093 created "2021-12-31" @default.
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• W4200544093 date "2022-01-12" @default.
• W4200544093 modified "2023-10-02" @default.
• W4200544093 title "Hypoxia‐inducible factor (HIF)‐1α‐induced regulation of lung injury in pulmonary aspiration is mediated through NF‐kB" @default.
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• W4200544093 doi "https://doi.org/10.1096/fba.2021-00132" @default.
• W4200544093 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35520392" @default.
• W4200544093 hasPublicationYear "2022" @default.
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