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Gut Microbes. 2014 Mar-Apr;5(2):254-8. doi: 10.4161/gmic.28093. Epub 2014 Feb 5.

SerpinB2 mediated regulation of macrophage function during enteric infection.

Author information

1
Department of Radiation Oncology; University of Maryland School of Medicine; Baltimore, MD USA; Department of Medicine; University of Maryland School of Medicine; Baltimore, MD USA; Department of Physiology; University of Maryland School of Medicine; Baltimore, MD USA.
2
Department of Radiation Oncology; University of Maryland School of Medicine; Baltimore, MD USA; Department of Medicine; University of Maryland School of Medicine; Baltimore, MD USA.
3
Department of Physiology; University of Maryland School of Medicine; Baltimore, MD USA; Center for Vascular and Inflammatory Diseases; University of Maryland School of Medicine; Baltimore, MD USA.

Abstract

Host defense is an orchestrated response involving changes in the expression of receptors and release of mediators from both immune and structural cells. There is a growing recognition of the important role of proteolytic pathways for the protective immune response to enteric pathogens. Enteric nematode infection induces a type 2 immune response with polarization of macrophages toward the alternatively activated phenotype (M2). The Th2 cytokines, IL-4, and IL-13, induce a STAT6-dependent upregulation of the expression of the protease inhibitor, serpinB2, which protects macrophages from apoptosis. M2 are critical to worm clearance and a novel role for serpinB2 is its regulation of the chemokine, CCL2, which is necessary for monocyte and/or macrophage influx into small intestine during infection. There is a growing list of factors including immune (LPS, Th2 cytokines) as well as hormonal (gastrin, 5-HT) that are linked to increased expression of serpinB2. Thus, serpinB2 represents an immune regulated factor that has multiple roles in the intestinal mucosa.

KEYWORDS:

Th2 cytokines; enteric nematode infection; macrophage; plasminogen activation system; serpinB2

PMID:
24637799
PMCID:
PMC4063854
DOI:
10.4161/gmic.28093
[Indexed for MEDLINE]
Free PMC Article

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