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• W3173670486 abstract "Neutrophil myeloperoxidase is a major mediator of microbicidal activity, catalyzing the conversion of hydrogen peroxide to hypochlorous acid (HOCl), a potent oxidant that reacts with both microbial and host molecular targets. HOCl targets the vinyl ether bond of plasmalogen lipids, resulting in the production of 2-chlorofatty aldehyde, which is in turn metabolized to 2-chlorofatty acid (2-ClFA). Recently, we have shown that free 2-ClFA levels are significantly associated with acute respiratory distress syndrome (ARDS) in sepsis patients. Lung endothelial cells treated with 2-ClFA showed increased permeability, surface expression of adhesion molecules, and neutrophil and platelet adherence. These data indicate that plasma 2-ClFA is a predictor for ARDS, likely through effects on the lung microvasculature. In this study, we determined the effect of 2-ClFA on human small airways epithelial cell (SAEC) function. Incubation of SAEC with 2-ClFA (100 nM-10 μM, up to 24 hours) resulted in a concentration- and time-dependent decrease in electrical resistance, with no change in resistance noted when SAEC were incubated with non-chlorinated fatty acid (FA). Our recently published studies published recently by us show that 2-ClFA (1 μM) treatment of lung microvascular endothelial cells resulted in a 2-fold increase in cell surface expression of intercellular adhesion molecule 1 (ICAM-1) and a 1.7-fold increase in vascular cell adhesion molecule 1 (VCAM-1) after a 4-hour incubation. We now show that incubation with 2-ClFA for 4 hours resulted in a 3.3-fold increase in cell surface expression of ICAM-1 and a 4.4-fold increase of VCAM-1 in SAEC. No increase in adhesion molecules was observed with FA incubation. 2-ClFA treatment resulted in neutrophil adherence to SAEC and enhanced transmigration across the SAEC monolayer after 2-ClFA treatment. Neutrophil transmigration across SAEC was 3-fold greater in a basolateral-to-apical direction when compared to apical-to-basolateral. Taken together, these data suggest that 2-ClFA mediates small airways epithelial dysfunction and neutrophil transmigration that may contribute to fluid accumulation and inflammation observed in ARDS patients. Support or Funding Information NIH R01 GM115553 (to D.A.F. and J.M.) This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal." @default.
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• W3173670486 date "2018-04-01" @default.
• W3173670486 modified "2023-09-24" @default.
• W3173670486 title "Chlorinated lipids mediate small airway epithelial dysfunction" @default.
• W3173670486 doi "https://doi.org/10.1096/fasebj.2018.32.1_supplement.286.2" @default.
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