Regulation of chemokine expression by XXXX in alveolar macrophages exposed to @entity519 and reoxygenation.

@entity9269 @entity4647 @entity5721 @entity870 @entity17104 @entity205 @entity519 @entity35 @entity647
BACKGROUND: We have recently demonstrated a role for selected chemokines in a @entity35 model of @entity5721 ( @entity5721 ). We have further shown that pretreatment with @entity205 ( @entity870 ) is protective. The precise cellular events regulating this model are unknown. The alveolar macrophage (AM) is a key effector cell in multiple models of @entity647 , and it likely plays a central role in @entity5721 as well. The present studies were undertaken to determine whether @entity870 functions in part by modifying the chemokine response of AMs to @entity519 and reoxygenation in vitro. METHODS: Alveola macrophages were rendered @entity519 (0.5%) for 2 hours and reoxygenated for 6 hours. The secreted chemokine content in the media was quantified by enzyme-linked immunosorbent assay, and nuclear protein was analyzed after electro-mobility shift assay. When employed, @entity870 was administered 30 minutes before @entity519 . RESULTS: Alveolar macrophages demonstrated a marked increase in the secretion of the chemokines, @entity17104 , @entity9269 , CINC, and @entity4647 , in response to @entity519 and reoxygenation. This increase was dependent on mRNA transcription and de novo protein synthesis. It was also blocked by a specific inhibitor of the nuclear translocation factor, NF-kappaB. Pretreatment with @entity870 (500 ng/mL) significantly reduced expression of chemokines and activation of NF-kappaB. CONCLUSIONS: @entity205 attenuates the chemokine response of AMs in vitro to @entity519 and reoxygenation at the pretranscriptional level through modulation of NF-kappaB. These findings suggest the potential mechanism of action of @entity870 's protective effects in @entity5721 .
