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Host defense peptide LL-37 selectively reduces proinflammatory macrophage responses.

Journal article
Authors Kelly Brown
Grace F T Poon
Darlene Birkenhead
Olga M Pena
Reza Falsafi
Claes Dahlgren
Anna Karlsson
Johan Bylund
Robert E W Hancock
Pauline Johnson
Published in Journal of immunology (Baltimore, Md. : 1950)
Volume 186
Issue 9
Pages 5497-505
ISSN 1550-6606
Publication year 2011
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 5497-505
Language en
Links dx.doi.org/10.4049/jimmunol.1002508
Subject categories Medical microbiology, Immunobiology

Abstract

The human cathelicidin peptide, LL-37, is a host defense peptide with a wide range of immunomodulatory activities and modest direct antimicrobial properties. LL-37 can exert both pro- and anti-inflammatory effects and can modulate the proinflammatory responses of human peripheral blood monocytes and epithelial cells. In this study, we evaluated the effect of LL-37 on mouse bone marrow-derived macrophages (BMDM) and tissue macrophages in vitro and in vivo. LL-37 dramatically reduced TNF-α and NO levels produced by LPS and IFN-γ-polarized M1-BMDM and slightly reduced reactive oxygen species production by these cells. LL-37 did not affect the ability of IL-4-polarized M2-BMDM to upregulate arginase activity, although it did inhibit LPS-induced TNF-α secretion in these cells. LL-37 did not compromise the ability of M1-polarized BMDM to phagocytose and kill bacteria and did not affect the uptake of apoptotic neutrophils by M2-polarized BMDM. However, LL-37-treated M1-BMDM were more efficient at suppressing tumor growth in vitro. LL-37 significantly reduced LPS-induced TNF-α secretion in ex vivo alveolar macrophages, whereas its effect on peritoneal macrophages was much less dramatic. Effective inhibition of LPS-induced TNF-α secretion by alveolar macrophages also occurred in vivo when LL-37 was administered by intratracheal injection. This demonstrates a selective ability of LL-37 to decrease M1-BMDM, M2-BMDM, and tissue macrophage production of the proinflammatory cytokine TNF-α in response to LPS while leaving other crucial anti-inflammatory M1 and M2 macrophage functions unaltered.

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