Lipopolysaccharide Induces @entity740 and XXXX through Activation of @entity3470 Signaling in Macrophages.

@entity1 @entity32 @entity8 @entity5694 @entity8929 @entity82 @entity17296 @entity295 @entity19 @entity635 @entity3124 @entity740 @entity3446 @entity3470 @entity130
BACKGROUND: Septic @entity8 is one of the most common complications in @entity3124 @entity1 with a high risk of developing @entity740 ( @entity740 ). Emerging data indicate that @entity1 target of rapamyci ( @entity3470 ) signaling plays a major role in septic @entity32 by regulating the immune response of macrophage. This study was designed to evaluate the role of @entity3470 signaling in kidney macrophages during @entity5694 -induced chronic @entity8 and subsequent fibrogenesis. METHODS: Male C57BL/6 @entity19 were used for all animal studies (n = 9 for each group). Lipopolysaccharide ( @entity17296 ) was injected intraperitoneally (1 mg/kg) every 2 days to induce persistent @entity5694 . @entity3446 (1 mg/kg  day) was administered to a subgroup of @entity19 1 day prior to @entity17296 treatment and continued to termination of the experiment. In ex-vivo experiment, RAW264.7 cells were cultured and treated with @entity17296 (2   g/ml) for 48 h while a subgroup of cells were incubated in the presence of @entity3446 (50 nmol) for 2 h. RESULTS: Continuous administration of @entity17296 resulted in progressive macrophage infiltration, tubular injury and collagen deposition in @entity19 kidneys. @entity3446 markedly ameliorated @entity17296 -induced kidney pathological changes. Expression of pS6K was rarely observed in normal kidney macrophages, but significantly increased with time by @entity17296 treatment. In ex-vivo study, @entity17296 induced prominent production of @entity635 and @entity8929 in cultured RAW264.7 cells, which was significantly suppressed by @entity3446 . CONCLUSION: Taken together, our findings show that @entity5694 results in activation of @entity3470 signaling in macrophages, leading to progressive kidney inflammatory @entity130 and subsequent @entity82 . Our study may reveal a mechanism involved in the development of @entity295 -associated @entity740 and @entity8 .
