title: Role of B cells in host defense against primary Coxiella burnetii infection.
abstract: Despite Coxiella burnetii being an obligate intracellular bacterial pathogen, our recent study demonstrated that B cells play a critical role in vaccine-induced immunity to C. burnetii infection by producing protective antibodies. However, the role of B cells in host defense against primary C. burnetii infection remains unclear. In this study, we investigated whether B cells play an important role in host defense against primary C. burnetii infection. The results showed that peritoneal B cells were able to phagocytose virulent C. burnetii bacteria and form Coxiella-containing vacuoles (CCVs) and that C. burnetii can infect and replicate in peritoneal B1a subset B cells in vitro, demonstrating a potential role for peritoneal B cells in host defense against C. burnetii infection in vivo. In addition, the results showing that B1a cells secreted a high level of interleukin-10 (IL-10) in response to C. burnetii infection in vitro suggest that B1a cells may play an important role in inhibiting the C. burnetii infection-induced inflammatory response. The observation that adoptive transfer of peritoneal B cells did not significantly affect the severity of C. burnetii infection-induced diseases in both severe combined immunity-deficient (SCID) and μMT mice indicates that peritoneal B cells alone may not be able to control C. burnetii infection. In contrast, our finding that C. burnetii infection induced more-severe splenomegaly and a higher bacterial burden in the spleens of B1a cell-deficient Bruton's tyrosine kinase x-linked immunity-deficient (BTK(xid)) mice than in their wild-type counterparts further suggests that B1a cells play an important role in host defense against primary C. burnetii infection.
authors.affiliation: Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Missouri-Columbia, Columbia, Missouri, USA.
authors.forename: Laura
authors.initials: L
authors.lastname: Schoenlaub
authors.affiliation: Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Missouri-Columbia, Columbia, Missouri, USA.
authors.forename: Alexandra
authors.initials: A
authors.lastname: Elliott
authors.affiliation: Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Missouri-Columbia, Columbia, Missouri, USA.
authors.forename: Danielle
authors.initials: D
authors.lastname: Freches
authors.affiliation: Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Missouri-Columbia, Columbia, Missouri, USA.
authors.forename: William J
authors.initials: WJ
authors.lastname: Mitchell
authors.affiliation: Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Missouri-Columbia, Columbia, Missouri, USA zhangguo@missouri.edu.
authors.forename: Guoquan
authors.initials: G
authors.lastname: Zhang
mesh_terms: D019264:Adoptive Transfer; D000077329:Agammaglobulinaemia Tyrosine Kinase; D000818:Animals; D016175:B-Lymphocyte Subsets / Q000276:immunology* / Q000382:microbiology / Q000473:pathology / Q000637:transplantation; D016997:Coxiella burnetii / Q000235:genetics* / Q000472:pathogenicity; D005260:Female; D015870:Gene Expression; D054884:Host-Pathogen Interactions / Q000276:immunology*; D056724:Immunity, Humoral; D016753:Interleukin-10 / Q000235:genetics / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D016513:Mice, SCID; D010587:Phagocytosis; D011505:Protein-Tyrosine Kinases / Q000172:deficiency / Q000235:genetics / Q000276:immunology; D011778:Q Fever / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D013154:Spleen / Q000276:immunology* / Q000382:microbiology / Q000473:pathology
chemical_list: C556062:IL10 protein, mouse; D016753:Interleukin-10; D011505:Protein-Tyrosine Kinases; D000077329:Agammaglobulinaemia Tyrosine Kinase; C000625951:Btk protein, mouse