NDLI: The C5a anaphylatoxin receptor (C5aR1) protects against Listeria monocytogenes infection by inhibiting type 1 IFN expression.

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The C5a anaphylatoxin receptor (C5aR1) protects against Listeria monocytogenes infection by inhibiting type 1 IFN expression.

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The C5a anaphylatoxin receptor (C5aR1) protects against Listeria monocytogenes infection by inhibiting type 1 IFN expression.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Morales, John E. Calame, Daniel G. Wetsel, Rick A. Mueller-Ortiz, Stacey L.
Description	Author Affiliation: Calame DG ( The Brown Foundation Institute of Molecular Medicine, Research Center for Immunology and Autoimmune Diseases, The University of Texas Health Science Center at Houston, Houston, TX 77030); Mueller-Ortiz SL ( The Brown Foundation Institute of Molecular Medicine, Research Center for Immunology and Autoimmune Diseases, The University of Texas Health Science Center at Houston, Houston, TX 77030); Morales JE ( The Brown Foundation Institute of Molecular Medicine, Research Center for Immunology and Autoimmune Diseases, The University of Texas Health Science Center at Houston, Houston, TX 77030); Wetsel RA ( The Brown Foundation Institute of Molecular Medicine, Research Center for Immunology and Autoimmune Diseases, The University of Texas Health Science Center at Houston, Houston, TX 77030)
Abstract	Listeria monocytogenes is a major cause of mortality resulting from food poisoning in the United States. In mice, C5 has been genetically linked to host resistance to listeriosis. Despite this genetic association, it remains poorly understood how C5 and its activation products, C5a and C5b, confer host protection to this Gram-positive intracellular bacterium. In this article, we show in a systemic infection model that the major receptor for C5a, C5aR1, is required for a normal robust host immune response against L. monocytogenes. In comparison with wild-type mice, C5aR1(-/-) mice had reduced survival and increased bacterial burden in their livers and spleens. Infected C5aR1(-/-) mice exhibited a dramatic reduction in all major subsets of splenocytes, which was associated with elevated caspase-3 activity and increased TUNEL staining. Because type 1 IFN has been reported to impede the host response to L. monocytogenes through the promotion of splenocyte death, we examined the effect of C5aR1 on type 1 IFN expression in vivo. Indeed, serum levels of IFN- and IFN-ß were significantly elevated in L. monocytogenes-infected C5aR1(-/-) mice. Similarly, the expression of TRAIL, a type 1 IFN target gene and a proapoptotic factor, was elevated in NK cells isolated from infected C5aR1(-/-) mice. Treatment of C5aR1(-/-) mice with a type 1 IFNR blocking Ab resulted in near-complete rescue of L. monocytogenes-induced mortality. Thus, these findings reveal a critical role for C5aR1 in host defense against L. monocytogenes through the suppression of type 1 IFN expression.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1401750
Journal	The Journal of Immunology
Issue Number	10
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-11-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Interferon-alpha Genetics Interferon-beta Listeria Monocytogenes Immunology Listeriosis Spleen Anaphylatoxins Animals Antibodies Pharmacology Apoptosis Bacterial Load Caspase 3 Complement C5a Complement C5b Gene Expression Drug Therapy Microbiology Mortality Liver Pathology Lymphocytes Mice Mice, Knockout Receptor, Anaphylatoxin C5a Receptors, Interferon Antagonists & Inhibitors Survival Analysis Tnf-related Apoptosis-inducing Ligand 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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