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α‐Melanocyte‐stimulating hormone inhibits lipopolysaccharide‐induced biological responses by downregulating CD14 from macrophages
Author(s) -
Sarkar Abira,
Sreenivasan Yashin,
Manna Sunil K
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)01029-9
Subject(s) - cd14 , lipopolysaccharide , tumor necrosis factor alpha , receptor , monocyte , inflammation , melanocyte stimulating hormone , chemistry , downregulation and upregulation , microbiology and biotechnology , cell adhesion molecule , endocrinology , medicine , biology , immunology , biochemistry , gene
Monocytes/macrophages are the first cells involved in inflammation. α‐Melanocyte‐stimulating hormone (α‐MSH) is known to possess an anti‐inflammatory role induced by a variety of stimuli; however, the molecular mechanisms underlying these effects are not clearly defined. In this report we provide evidence that α‐MSH inhibited serum‐activated lipopolysaccharide (SA‐LPS)‐induced proteolytic enzyme release, oxidative burst response, reactive oxygen intermediate generation, nitric oxide production, and adhesion molecule expression in monocyte‐derived macrophages. α‐MSH also inhibited SA‐LPS‐induced nuclear transcription factor κB activation not only in macrophages, but also in a T‐cell line and human neutrophils isolated from fresh blood. α‐MSH downregulated CD14, but not interleukin‐1 receptor, tumor necrosis factor receptor 1 or 2 from the surface of macrophages. Anti‐CD14 antibody was unable to protect α‐MSH‐mediated downregulation of CD14. Overall, our results suggest that α‐MSH exerts its anti‐inflammatory effect by a novel mechanism in macrophages through downregulating of the endotoxin receptor CD14.