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Infection and Immunity, April 2001, p. 2345-2352, Vol. 69, No. 4
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.4.2345-2352.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Interleukin-10 Stimulates Coxiella burnetii Replication in Human Monocytes through Tumor Necrosis Factor Down-Modulation: Role in Microbicidal Defect of Q Fever

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

Unité des Rickettsies, CNRS UMR 6020, Université de la Méditerranée, Marseille, France

Received 20 November 2000/Returned for modification 19 December 2000/Accepted 19 January 2001

Coxiella burnetii, an obligate intracellular bacterium, is the agent of Q fever. The chronic form of the disease is associated with the overproduction of interleukin-10 and deficient C. burnetii killing by monocytes. We hypothesized that the replication of C. burnetii inside monocytes requires a macrophage-deactivating cytokine such as interleukin-10. In the absence of interleukin-10, C. burnetii survived but did not replicate in monocytes. C. burnetii replication (measured 15 days) was induced in interleukin-10-treated monocytes. This effect of interleukin-10 is specific since transforming growth factor beta 1 had no effect on bacterial replication. C. burnetii replication involves the down-modulation of tumor necrosis factor (TNF) release. First, interleukin-10 suppressed C. burnetii-stimulated production of TNF. Second, the addition of recombinant TNF to interleukin-10-treated monocytes inhibited bacterial replication. Third, the incubation of infected monocytes with neutralizing anti-TNF antibodies favored C. burnetii replication. On the other hand, deficient C. burnetii killing by monocytes from patients with chronic Q fever involves interleukin-10. Indeed, C. burnetii replication was observed in monocytes from patients with Q fever endocarditis, but not in those from patients with acute Q fever. Bacterial replication was inhibited by neutralizing anti-interleukin-10 antibodies. As monocytes from patients with endocarditis overproduced interleukin-10, the defective bacterial killing is likely related to endogenous interleukin-10. These results suggest that interleukin-10 enables monocytes to support C. burnetii replication and to favor the development of chronic Q fever.

* Corresponding author. Mailing address: Unité des Rickettsies, CNRS UMR 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, April 2001, p. 2345-2352, Vol. 69, No. 4
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.4.2345-2352.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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