Sepsis induces incomplete M2 phenotype polarization in peritoneal exudate cells in miceReport as inadecuate




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Journal of Intensive Care

, 4:6

First Online: 12 January 2016Received: 04 August 2015Accepted: 29 December 2015

Abstract

BackgroundMacrophages can differentiate into pro-inflammatory M1 or anti-inflammatory M2 phenotypes upon exposure to a pathogen or a cytokine microenvironment. However, M1-M2 macrophage polarization in polymicrobial sepsis has not been fully characterized.

MethodsThe polarity of peritoneal exudate PE cells from mice that had undergone cecal ligation and puncture CLP and the response of those cells to lipopolysaccharide LPS in terms of cytokine and chemokine expression were examined.

ResultsPE cells from CLP mice demonstrated a shift toward the M2 phenotype in terms of marker enzyme expression. In addition, the CLP-derived PE cells showed apparent unresponsiveness to LPS stimulation with regard to expression of pro-inflammatory cytokines such as TNF-α, while the expression of anti-inflammatory cytokines such as IL-10 was induced. Nevertheless, the CLP-PE cells failed to express M2 chemokines including chemokine C-C motif ligand 17 CCL17, CCL22, and CCL24, all of which are important for T cell recruitment.

ConclusionsThe results suggested that a shift of naïve monocytes-macrophages to the M2 phenotype, along with the lack of M2 chemokine expression in septic monocytes-macrophages, might be responsible for immunosuppression after sepsis.

KeywordsMacrophage Immunosuppression Secondary infection Sepsis AbbreviationsARGarginase

CCLchemokine C-C motif ligand

CLPcecal ligation and puncture

ILinterleukin

iNOSinducible nitric oxide synthase

LPSlipopolysaccharide

MCPmonocyte chemoattractant protein

PEperitoneal exudate

SOCSsuppressor of cytokine signaling

Electronic supplementary materialThe online version of this article doi:10.1186-s40560-015-0124-1 contains supplementary material, which is available to authorized users.

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Author: Nobuo Watanabe - Yusuke Suzuki - Sadaki Inokuchi - Shigeaki Inoue

Source: https://link.springer.com/







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