UP-REGULATION OF TUMOR-NECROSIS-FACTOR-ALPHA AND INTERLEUKIN-1-BETA IN Q-FEVER ENDOCARDITIS

The occurrence of Q fever endocarditis likely involves some alteration s in the responses of monocytes, the in vivo targets of Coxiella burne tii. To test this hypothesis, the production of the inflammatory cytok ines tumor necrosis factor alpha, interleukin-1 beta, and interleukin- 6 was assessed in monocytes from patients with Q fever endocarditis. S pontaneous transcription and secretion of tumor necrosis factor and in terleukin-1 were significantly higher in patient monocytes than in hea lthy controls. The interleukin-6 transcripts were also upregulated in patient cells. Moreover, in patients with recent endocarditis exhibiti ng high titers of immunoglobulin G directed to C. burnetii in phase I, monocytes released significantly higher levels of tumor necrosis fact or and interleukin-1 than in patients with stabilized endocarditis. Im munoglobulin G titers and the overproduction of tumor necrosis factor and interleukin-1 were significantly correlated. Hence, the overproduc tion of inflammatory cytokines might be a marker of disease activity.