Homeostatic regulation of Salmonella-induced mucosal inflammation and injury by IL-23.

Abstract	IL-12 and IL-23 regulate innate and adaptive immunity to microbial pathogens through influencing the expression of IFN-γ, IL-17, and IL-22. Herein we define the roles of IL-12 and IL-23 in regulating host resistance and intestinal inflammation during acute Salmonella infection. We find that IL-23 alone is dispensable for protection against systemic spread of bacteria, but synergizes with IL-12 for optimal protection. IL-12 promotes the production of IFN-γ by NK cells, which is required for resistance against Salmonella and also for induction of intestinal inflammation and epithelial injury. In contrast, IL-23 controls the severity of inflammation by inhibiting IL-12A expression, reducing IFN-γ and preventing excessive mucosal injury. Our studies demonstrate that IL-23 is a homeostatic regulator of IL-12-dependent, IFN-γ-mediated intestinal inflammation.
Authors	Muyiwa Awoniyi, Samuel I Miller, Christopher B Wilson, Adeline M Hajjar, Kelly D Smith
Journal	PloS one (PLoS One) Vol. 7 Issue 5 Pg. e37311 ( 2012) ISSN: 1932-6203 [Electronic] United States
PMID	22624013 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)
Chemical References	Il17rc protein, mouse Il23a protein, mouse Interleukin-23 Subunit p19 Interleukins Receptors, Interleukin Interleukin-12 Interferon-gamma interleukin-22
Topics	Analysis of Variance Animals Female Flow Cytometry Gene Expression Regulation (immunology) Homeostasis (immunology) Immunohistochemistry Interferon-gamma (genetics, immunology) Interleukin-12 (genetics, immunology) Interleukin-23 Subunit p19 (genetics, immunology) Interleukins (genetics, immunology) Intestinal Mucosa (immunology, microbiology, pathology) Male Mice Mice, Inbred C57BL Mice, Knockout Real-Time Polymerase Chain Reaction Receptors, Interleukin (genetics, immunology) Salmonella Infections (immunology, pathology) Salmonella typhimurium (immunology)

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