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Despite the importance of the innate immune system in fighting L. monocytogenes infection, little is known about the role of complement and its activation products, including the potent C3a anaphylatoxin. In a model of systemic L. monocytogenes infection, we show that mice lacking the receptor for C3a (C3aR\u2212\/\u2212) are significantly more sensitive to infection compared with wild-type mice, as demonstrated by decreased survival, increased bacterial burden, and increased damage to their livers and spleens. The inability of the C3aR\u2212\/\u2212 mice to clear the bacterial infection was not caused by defective macrophages or by a reduction in cytokines\/chemokines known to be critical in the host response to L. monocytogenes, including IFN-\u03b3 and TNF-\u03b1. Instead, TUNEL staining, together with Fas, active caspase-3, and Bcl-2 expression data, indicates that the increased susceptibility of C3aR\u2212\/\u2212 mice to L. monocytogenes infection was largely caused by increased L. monocytogenes\u2013induced apoptosis of myeloid and lymphoid cells in the spleen that are required for ultimate clearance of L. monocytogenes, including neutrophils, macrophages, dendritic cells, and T cells. These findings reveal an unexpected function of C3a\/C3aR signaling during the host immune response that suppresses Fas expression and caspase-3 activity while increasing Bcl-2 expression, thereby providing protection to both myeloid and lymphoid cells against L. monocytogenes\u2013induced apoptosis.<\/jats:p>","DOI":"10.4049\/jimmunol.1302787","type":"journal-article","created":{"date-parts":[[2014,7,1]],"date-time":"2014-07-01T14:20:47Z","timestamp":1404224447000},"page":"1278-1289","source":"Crossref","is-referenced-by-count":37,"title":["The Receptor for the Complement C3a Anaphylatoxin (C3aR) Provides Host Protection against <i>Listeria monocytogenes<\/i>\u2013Induced Apoptosis"],"prefix":"10.1093","volume":"193","author":[{"given":"Stacey L","family":"Mueller-Ortiz","sequence":"first","affiliation":[{"name":"Brown Foundation Institute of Molecular Medicine, Research Center for Immunology and Autoimmune Diseases, University of Texas Medical School at Houston , Houston, TX 77030"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John E","family":"Morales","sequence":"additional","affiliation":[{"name":"Brown Foundation Institute of Molecular Medicine, Research Center for Immunology and Autoimmune Diseases, University of Texas Medical School at Houston , Houston, TX 77030"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rick A","family":"Wetsel","sequence":"additional","affiliation":[{"name":"Brown Foundation Institute of Molecular Medicine, Research Center for Immunology and Autoimmune Diseases, University of Texas Medical School at Houston , Houston, TX 77030"},{"name":"Department of Biochemistry and Molecular Biology, University of Texas Medical School at Houston , Houston, TX 77030"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2014,8,1]]},"reference":[{"key":"2025030707250204900_r1","doi-asserted-by":"crossref","first-page":"S18","DOI":"10.1086\/338465","article-title":"Listeria monocytogenes: clinical and experimental update","volume":"185","author":"Wing","year":"2002","journal-title":"J. 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