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Thrombospondin\u20101 (TSP\u20101) is specifically upregulated in several inflammatory diseases and can effectively promote lipopolysaccharide\u2010 (LPS\u2010) induced inflammation. In contrast, thrombospondin\u20102 (TSP\u20102) has been associated with activation of \u201canti\u2010inflammatory\u201d T\u2010regulatory cells (Tregs). In this study, we investigated the effects of both TSP\u20101 and TSP\u20102 overexpression on macrophage polarization and activation <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic>. We analyzed the effects of TSP\u20101 and TSP\u20102 on inflammation, vascular endothelial permeability, edema, ultrastructural morphology, and apoptosis in lung tissues of an ARDS mouse model and cultured macrophages. Our results demonstrated that TSP\u20102 overexpression effectively attenuated LPS\u2010induced ARDS <jats:italic>in vivo<\/jats:italic> and promoted M2 macrophage phenotype polarization <jats:italic>in vitro<\/jats:italic>. Furthermore, TSP\u20102 played a role in regulating pulmonary vascular barrier leakage by activating the PI3K\/Akt pathway. Overall, our findings indicate that TSP\u20102 can modulate inflammation and could therefore be a potential therapeutic target against LPS\u2010induced ARDS.<\/jats:p>","DOI":"10.1155\/2021\/8876484","type":"journal-article","created":{"date-parts":[[2021,4,17]],"date-time":"2021-04-17T15:05:10Z","timestamp":1618671910000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Contribution of Thrombospondin\u20101 and \u20102 to Lipopolysaccharide\u2010Induced Acute Respiratory Distress 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