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Infect. Immun., May 1996, 1638-1642, Vol 64, No. 5
C Capo, F Zugun, A Stein, G Tardei, H Lepidi, D Raoult and JL Mege
The occurrence of Q fever endocarditis likely involves some alterations in
the responses of monocytes, the in vivo targets of Coxiella burnetii. To
test this hypothesis, the production of the inflammatory cytokines tumor
necrosis factor alpha, interleukin-1 beta, and interleukin-6 was assessed
in monocytes from patients with Q fever endocarditis. Spontaneous
transcription and secretion of tumor necrosis factor and interleukin-1 were
significantly higher in patient monocytes than in healthy controls. The
interleukin-6 transcripts were also upregulated in patient cells. Moreover,
in patients with recent endocarditis exhibiting high titers of
immunoglobulin G directed to C. burnetii in phase I, monocytes released
significantly higher levels of tumor necrosis factor and interleukin-1 than
in patients with stabilized endocarditis. Immunoglobulin G titers and the
overproduction of tumor necrosis factor and interleukin-1 were
significantly correlated. Hence, the overproduction of inflammatory
cytokines might be a marker of disease activity.
Copyright © 1996, American Society for Microbiology
Upregulation of tumor necrosis factor alpha and interleukin-1 beta in Q fever endocarditis
Unite des Rickettsies, Centre National de la Recherche Scientifique EPJ 0054, Marseille, France.
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