NDLI: Activation of the epidermal growth factor receptor in macrophages regulates cytokine production and experimental colitis.

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Activation of the epidermal growth factor receptor in macrophages regulates cytokine production and experimental colitis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Cao, Hailong Wilson, Keith T. Washington, Mary K. Rosen, Michael J. Polk, D. Brent Hao, Xishan Liu, Liping Yan, Fang Dubé, Philip E. Wang, Lihong Van Kaer, Luc Ren, Xiubao Lu, Ning
Description	Author Affiliation: Lu N ( Department of Breast Cancer Medical Oncology, Key Laboratory of Breast Cancer Prevention and Therapy, Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Tianjin 300060, P. R. China)
Abstract	Macrophages regulate innate immunity to maintain intestinal homeostasis and play pathological roles in intestinal inflammation. Activation of the epidermal growth factor receptor (EGFR) promotes cellular proliferation, differentiation, survival, and wound closure in several cell types. However, the impact of EGFR in macrophages remains unclear. This study was to investigate whether EGFR activation in macrophages regulates cytokine production and intestinal inflammation. We found that EGFR was activated in colonic macrophages in mice with dextran sulfate sodium (DSS)-induced colitis and in patients with ulcerative colitis. DSS-induced acute colitis was ameliorated, and recovery from colitis was promoted in Egfr(fl/fl)LysM-Cre mice with myeloid cell-specific deletion of EGFR, compared with LysM-Cre mice. DSS treatment increased IL-10 and TNF levels during the acute phase of colitis, and increased IL-10 but reduced TNF levels during the recovery phase in Egfr(fl/fl)LysM-Cre mice. An anti-IL-10 neutralizing Ab abolished these effects of macrophage-specific EGFR deletion on DSS-induced colitis in Egfr(fl/fl)LysM-Cre mice. LPS stimulated EGFR activation and inhibition of EGFR kinase activity enhanced LPS-stimulated NF-κB activation in RAW 264.7 macrophages. Furthermore, induction of IL-10 production by EGFR kinase-blocked RAW 264.7 cells, in response to LPS plus IFN-Î³, correlated with decreased TNF production. Thus, although selective deletion of EGFR in macrophages leads to increases in both pro- and anti-inflammatory cytokines in response to inflammatory stimuli, the increase in the IL-10 level plays a role in suppressing proinflammatory cytokine production, resulting in protection of mice from intestinal inflammation. These results reveal an integrated response of macrophages regulated by EGFR in intestinal inflammatory disorders.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1300133
Journal	The Journal of Immunology
Issue Number	3
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Colitis Immunology Cytokines Biosynthesis Macrophages Receptor, Epidermal Growth Factor Physiology Adolescent Animals Cell Line Chemically Induced Metabolism Colitis, Ulcerative Colon Pathology Cyclooxygenase 2 Genetics Dextran Sulfate Toxicity Gene Expression Regulation Immunity, Innate Inflammation Interferon-gamma Pharmacology Interleukin-10 Antagonists & Inhibitors Lipopolysaccharides Macrophage Activation Mice Mice, Inbred C57bl Myeloid Cells Nf-kappa B Neutrophils Quinazolines Deficiency Regeneration Signal Transduction Spleen Tumor Necrosis Factor-alpha Tyrphostins Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Activation of the epidermal growth factor receptor in macrophages regulates cytokine production and experimental colitis.

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