XXXX superimposed on aging magnifies @entity32 and delays the resolving response after @entity583 .

@entity5204 @entity32 @entity25084 @entity28 @entity19 @entity1426 @entity14636 @entity11903 @entity6580 @entity583 @entity10873 @entity1996 @entity446 @entity1446
@entity5204 ( @entity5204 ) intake has increased over the last 100 yr, contributing to the current obesogenic environment. @entity28 and aging are prominent risk factors for @entity583 ( @entity583 ). How @entity28 interacts with aging to alter the post- @entity583 response, however, is unclear. We tested the hypothesis that @entity28 in aging @entity19 would impair the resolution of @entity583 . @entity5204 diet ( @entity5204 aging group) feeding to 12-mo-old C57BL/6J @entity19 for 5 mo showed higher fat mass compared with standard lab chow (LC)-fed young (LC young group; 3-5 mo old) or aging alone control @entity19 (LC aging group). LC young, LC aging, and @entity5204 aging @entity19 were subjected to coronary artery ligation to induce @entity583 . Despite similar @entity583 , plasma proteomic profiling revealed higher @entity6580 in the @entity5204 aging group compared with LC young and LC aging groups, leading to increased neutrophil infiltration in the @entity5204 aging group (P<0.05). Macrophage inflammatory protein-1y and @entity14636 were also increased at day 1, and @entity10873 remained elevated at day 5, an observation consistent with delayed wound @entity446 in the @entity5204 aging group. Lipidomic analysis showed higher levels of @entity1426 and @entity11903 at day 1 post- @entity583 in the @entity5204 aging group compared with the LC aging group (all P<0.05), thereby mediating neutrophil extravasation in the @entity5204 aging group. The @entity32 -resolving enzymes @entity25084 , @entity1996 , and @entity1446 oxyegnase-1 were altered to delay wound @entity583 in the @entity5204 aging group compared with LC young and LC aging groups. @entity5204 aging magnifies the post- @entity583 inflammatory response and impairs the @entity446 response by stimulating prolonged neutrophil trafficking and proinflammatory lipid mediators.
