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LPS induces pulmonary intravascular macrophages producing inflammatory mediators via activating NF‐κB
Author(s) -
Chen ZhengTang,
Li ShengLiang,
Cai EnQi,
Wu WeiLing,
Jin JingSheng,
Zhu Bo
Publication year - 2003
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.10590
Subject(s) - nf κb , inflammation , microbiology and biotechnology , nfkb1 , chemistry , macrophage , immunology , medicine , biology , transcription factor , in vitro , biochemistry , gene
Pulmonary intravascular macrophages (PIMs) are often responsible for the clearance of blood‐borne pathogens, including endotoxin, lipopolysaccharide of Gram‐negative bacteria. It is well accepted that PIMs play a pivotal role in the pathogenesis of endotoxin‐induced acute lung injury. However, the mechanisms by which PIMs are involved in the lipopolysaccharide‐induced inflammatory responses remain unclear. Through the present study the following results were found: (1) When challenged with lipopolysaccharide (10 μg/ml), PIMs underwent marked cellular enlargement, intercellular adhesion plaques became longer, and some particulates were enwrapped in the pseudopods. (2) Lipopolysaccharide could up‐regulate the expression of some inflammatory mediators in PIMs, including TNF‐α, IL‐1β, IL‐6, IL‐8, and COX‐2, and these up‐regulated expression of inflammatory mediators correlated with NF‐κB activation. (3) Dexamethasone as well as acetylsalicylic acid reduced the expression of TNF‐α in lipopolysaccharide‐challenged PIMs, and the decreased expression of TNF‐α was also consistent with decreased NF‐κB activation. Our results suggest that NF‐κB activation in PIMs followed by phagocytizing lipopolysaccharide resulted in the up‐regulation of TNF‐α, IL‐1β, IL‐6, IL‐8, and COX‐2, which could be alleviated by dexamethasone. © 2003 Wiley‐Liss, Inc.