| Autor: |
Dellacasagrande, Jérôme, Ghigo, Eric, Capo, Christian, Raoult, Didier, Mege, Jean-Louis |
| Zdroj: |
Infection and Immunity; January 2000, Vol. 68 Issue: 1 p160-164, 5p |
| Abstrakt: |
ABSTRACTEndocarditis 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. burnetiiby monocytes. Monocytes from healthy controls eliminated virulent C. burnetiiwithin 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. burnetiias did control cells. The addition of supernatants ofC. burnetii-stimulated monocytes from patients with ongoing endocarditis to control monocytes enabled them to support C. burnetiisurvival, 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. burnetiiin patients with ongoing endocarditis compared to cured patients and healthy controls. In addition, neutralizing anti-TNF antibodies decreased C. burnetiiinternalization, 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 ofC. burnetiiby modulating early phases of microbial killing. |
| Databáze: |
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