title: T cells are essential for bacterial clearance, and gamma interferon, tumor necrosis factor alpha, and B cells are crucial for disease development in Coxiella burnetii infection in mice.
abstract: Coxiella burnetii, the etiological agent of Q fever, has two phase variants. Phase I has a complete lipopolysaccharide (LPS), is highly virulent, and causes Q fever in humans and pathology in experimental animals. Phase II lacks an LPS O side chain, is avirulent, and does not grow well in immunocompetent animals. To understand the pathogenicity of Q fever, we investigated the roles of immune components in animals infected with Nine Mile phase I (NM I) or Nine Mile phase II (NM II) bacteria. Immunodeficient mice, including SCID mice (deficient in T and B cells), SCIDbg mice (deficient in T, B, and NK cells), nude mice (deficient in T cells), muMT mice (deficient in B cells), bg mice (deficient in NK cells), mice deficient in tumor necrosis factor alpha (TNF-alpha(-/-) mice), and mice deficient in gamma interferon (IFN-gamma(-/-) mice), were compared for their responses to infection. SCID, SCIDbg, nude, and IFN-gamma(-/-) mice showed high susceptibility to NM I, and TNF-alpha(-/-) mice showed modest susceptibility. Disease caused by NM I in SCID, SCIDbg, and nude mice progressed slowly, while disease in IFN-gamma(-/-) and TNF-alpha(-/-) mice advanced rapidly. B- and NK-cell deficiencies did not enhance clinical disease development or alter bacterial clearance but did increase the severity of histopathological changes, particularly in the absence of B cells. Mice infected with NM II showed no apparent clinical disease, but T-cell-deficient mice had histopathological changes. These results suggest that T cells are critical for clearance of C. burnetii, either NM I or NM II, that IFN-gamma and TNF-alpha are essential for the early control of infection, and that B cells are important for the prevention of tissue damage.
authors: Department of Microbial and Molecular Pathogenesis, Texas A&M Health Science Center, College Station, TX 77843-1114, USA.
authors: Masako
authors: M
authors: Andoh
authors: Guoquan
authors: G
authors: Zhang
authors: Kasi E
authors: KE
authors: Russell-Lodrigue
authors: Heather R
authors: HR
authors: Shive
authors: Brad R
authors: BR
authors: Weeks
authors: James E
authors: JE
authors: Samuel
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D002460:Cell Line; D002642:Chick Embryo; D016997:Coxiella burnetii / Q000145:classification / Q000276:immunology / Q000472:pathogenicity*; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis* / Q000172:deficiency / Q000235:genetics; D008070:Lipopolysaccharides / Q000378:metabolism; D008099:Liver / Q000382:microbiology / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D008819:Mice, Nude; D016513:Mice, SCID; D011778:Q Fever / Q000276:immunology* / Q000382:microbiology / Q000401:mortality / Q000473:pathology; D013154:Spleen / Q000382:microbiology / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000172:deficiency / Q000235:genetics; D014774:Virulence
chemical_list: D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma