Injection of inactivated phase I Coxiella burnetii increases non-specific resistance to infection and stimulates lymphokine production in mice.
The encounter of phase I C. burnetii with the host results in seemingly disparate consequences. On the one hand, in vitro lymphocyte responses to mitogens and homologous recall antigen are suppressed. On the other, host resistance to a variety of infectious agents and to a tumor is increased. An explanation for this augmented immune response surely involves the ability of C. burnetii to stimulate cytokines, such as interferon and TNF, which enhance host immune function.
United States Army Medical Research Institute of Infectious Diseases, Department of Intracellular Pathogens, Fort Detrick, Frederick, Maryland 21701-5011.
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D000818:Animals; D003381:Coxiella / Q000276:immunology*; D007113:Immunity, Innate; D007372:Interferons / Q000096:biosynthesis*; D007942:Leukemia, Experimental / Q000276:immunology; D008088:Listeriosis / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011008:Pneumococcal Infections / Q000276:immunology; D011778:Q Fever / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*; D014777:Virus Diseases / Q000276:immunology
D014409:Tumor Necrosis Factor-alpha; D007372:Interferons