@entity1851 polarizes XXXX macrophages to an M1 phenotype and inhibits transformation to the M2 phenotype.

@entity1 @entity222 @entity10685 @entity2939 @entity5 @entity310 @entity3646 @entity2842 @entity1192 @entity35 @entity731 @entity1851
OBJECTIVE: Inflammation is pivotal in @entity731 . Monocyte-macrophages are crucial in @entity731 . Monocytes can develop into subsets: classically (M1) or alternatively (M2) activated cells. Several studies point to a proinflammatory role for @entity1851 (CRP). Because there is a paucity of data on the effects of CRP on macrophage phenotype, we tested effects of CRP on macrophage polarization. METHODS AND RESULTS: Monocytes were incubated with CRP (0 to 50  g/mL) and differentiated into macrophages for 7 days. Phenotypic characterization of M1 and M2 macrophages was performed using flow cytometry. CRP treatment resulted in increased population of M1 macrophages ( @entity5 necrosis factor [TNF]/interleukin [IL]-12/C-C chemokine receptor 2, TNF/IL-12/ @entity2842 , or TNF/ @entity1192 /IL-12). These effects were not abrogated by polymixin B or small interfering RNA to @entity2939 , but they were abrogated by boiled CRP. Administration of @entity1 CRP to @entity35 in vivo increased polarization of macrophages to M1 phenotype compared with human serum albumin. When macrophages were primed to the M2 phenotype with @entity3646 , addition of CRP resulted in significantly increased secretion of @entity310 , @entity2842 , and @entity1192 and conversion of macrophages from the M2 to the M1 phenotype. CRP failed to prime macrophages to the M1 phenotype in presence of @entity222 / @entity10685 small interfering RNA or dominant-negative nuclear factor kappa B. CONCLUSION: Collectively, these results further support a role for CRP in promoting differentiation of @entity1 monocytes toward a proinflammatory M1 phenotype.
