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• W4317548784 endingPage "152048" @default.
• W4317548784 startingPage "152048" @default.
• W4317548784 abstract "Surfactant protein D (SP-D) is an innate host defense protein that clears infectious pathogens from the lung and regulates pulmonary host defense cells. SP-D is also detected in lower concentrations in plasma and many other non-pulmonary tissues. Plasma levels of SP-D increase during infection and other proinflammatory states; however, the source and functions of SP-D in the systemic circulation are largely unknown. We hypothesized that systemic SP-D may clear infectious pathogens and regulate host defense cells in extrapulmonary systems.To determine if SP-D inhibited inflammation induced by systemic lipopolysaccharide (LPS), E.coli LPS was administered to mice via tail vein injection with and without SP-D and the inflammatory response was measured.Systemic SP-D has a circulating half-life of 6 h. Systemic IL-6 levels in mice lacking the SP-D gene were similar to wild type mice at baseline but were significantly higher than wild type mice following LPS treatment (38,000 vs 29,900 ng/ml for 20 mg/kg LPS and 100,700 vs 73,700 ng/ml for 40 mg/kg LPS). In addition, treating wild type mice with purified intravenous SP-D inhibited LPS induced secretion of IL-6 and TNFα in a concentration dependent manner. Inhibition of LPS induced inflammation by SP-D correlated with SP-D LPS binding suggesting SP-D mediated inhibition of systemic LPS requires direct SP-D LPS interactions.Taken together, the above results suggest that circulating SP-D decreases systemic inflammation and raise the possibility that a physiological purpose of increasing systemic SP-D levels during infection is to scavenge systemic infectious pathogens and limit inflammation-induced tissue injury." @default.
• W4317548784 created "2023-01-20" @default.
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• W4317548784 date "2023-04-01" @default.
• W4317548784 modified "2023-09-27" @default.
• W4317548784 title "Intravenous surfactant protein D inhibits lipopolysaccharide-induced systemic inflammation" @default.
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• W4317548784 doi "https://doi.org/10.1016/j.aanat.2023.152048" @default.
• W4317548784 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36690045" @default.
• W4317548784 hasPublicationYear "2023" @default.
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