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Infection and Immunity, January 2000, p. 160-164, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Coxiella burnetii Survives in Monocytes from Patients with Q Fever Endocarditis: Involvement of Tumor Necrosis Factor

Jérôme Dellacasagrande, Eric Ghigo, Christian Capo, Didier Raoult, and Jean-Louis Mege*

Unité des Rickettsies, Université de la Méditerranée, CNRS UPRESA 6020, Faculté de Médecine, 13385 Marseille Cedex 05, France

Received 22 July 1999/Returned for modification 1 September 1999/Accepted 5 October 1999

Endocarditis is the most frequent form of chronic Q fever, an infectious disease caused by Coxiella burnetii. As this obligate intracellular bacterium inhabits monocytes and macrophages, we wondered if pathogenesis of Q fever endocarditis is related to defective intracellular killing of C. burnetii by monocytes. Monocytes from healthy controls eliminated virulent C. burnetii within 3 days. In contrast, monocytes from patients with ongoing Q fever endocarditis were unable to eliminate bacteria even after 6 days. In patients who were cured of endocarditis, the monocyte infection was close to that of control monocytes. This killing deficiency was not the consequence of generalized functional impairment, since patient monocytes eliminated avirulent C. burnetii as did control cells. The addition of supernatants of C. burnetii-stimulated monocytes from patients with ongoing endocarditis to control monocytes enabled them to support C. burnetii survival, suggesting that some soluble factor is responsible for bacterial survival. This factor was related to tumor necrosis factor (TNF): expression of TNF mRNA and TNF release were increased in response to C. burnetii in patients with ongoing endocarditis compared to cured patients and healthy controls. In addition, neutralizing anti-TNF antibodies decreased C. burnetii internalization, an early step of bacterial killing, in monocytes from patients with ongoing endocarditis but did not affect delayed steps of intracellular killing. We suggest that Q fever-associated activation of monocytes allows the survival of C. burnetii by modulating early phases of microbial killing.

* Corresponding author. Mailing address: Unité des Rickettsies, CNRS UPRESA 6020, Faculté de Médecine, 27 Bd J. Moulin, 13385 Marseille Cedex 05, France. Phone: (33) 4 91 32 43 75. Fax: (33) 4 91 38 77 72. E-mail: Jean-Louis.Mege{at}medecine.univ-mrs.fr.

Infection and Immunity, January 2000, p. 160-164, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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