ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
TMEM16F deficiency alleviates sepsis-induced acute lung injury through regulating macrophage polarization.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundSepsis-induced acute lung injury (ALI) is closely associated with the balance of M1/M2 macrophage polarization and excessive inflammation. Recently studies have revealed that TMEM16F, a calcium-activated phospholipid scramblase, participates in modulating inflammatory response and oxidative stress. However, the effect of TMEM16F on regulation of M1/M2 polarization during sepsis-induced ALI and its underlying mechanisms remain unclear.
methodsIn the present study, we utilized septic patients, lipopolysaccharide (LPS)-induced ALI mouse models, and LPS-treated mouse alveolar macrophages (AMs) as well as human THP-1-derived macrophages to investigate the potential functions and molecular mechanisms of TMEM16F in sepsis-induced ALI.
resultsOur clinical analysis showed that TMEM16F mRNA levels in peripheral blood mononuclear cells (PBMCs) were positively correlated with inflammation and disease severity in septic patients. Additionally, TMEM16F was highly expressed in LPS-treated THP-1 macrophages and in vitro sepsis-induced ALI models. TMEM16F knockout significantly promoted M2 macrophage polarization, alleviated systemic inflammation, lung injury, oxidative stress and microthrombosis, and improved survival in septic mice. Mechanistically, TMEM16F could interact with SOCS3, suppressing downstream STAT3 signaling pathway and promoting NLRP3 inflammasome activation, resulting in increased M1 polarization and inflammatory response. Moreover, we identified platycodin D (PLD), a saponin found from Platycodon grandiflorum, could be an effective inhibitor of TMEM16F, and ameliorate sepsis-induced ALI by reprogramming macrophages towards an anti-inflammatory phenotype via inhibiting TMEM16F-mediated SOCS3/STAT3/NLRP3 pathway.
conclusionsCollectively, these findings indicated that TMEM16F plays a crucial role in regulating macrophage phenotypic switching, and highlighted targeting TMEM16F is a therapeutic strategy for attenuating sepsis-associated ALI through immune homeostasis restoration.
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