Production of interleukin-10 and transforming growth factor beta by peripheral blood mononuclear cells in Q fever endocarditis

The pathophysiology of Q fever endocarditis is characterized by the suppression of antigen-specific cell-mediated immune responses, We investigated the production of interleukin-10 (IL-10) and transforming growth factor beta (TGF-beta), known to interfere with the development of protective cell immunity, IL-10 was markedly released by unstimulated peripheral blood mononuclear cells (PBMC) from patients with Q fever endocarditis. This release resulted from the upregulation of IL-10 gene transcription, Similarly, the release of TGF-beta 1 and TGF-beta 2 was significantly higher in patient PBMC than in control cells, but the expression of their respective mRNA was not enhanced in patient cells, In contrast, lipopolysaccharide-stimulated transcription and release of IL-10 and TGF-beta were similar in patients and controls, The release of IL-10 by PBMC but not that of TGF-beta was correlated with the clinical status of the patients, First, IL-10 production was correlated with specific antibody levels, Second, IL-10 release remained elevated in patients prone to relapse, Taken together, our results suggest that the release of IL-10 and TGF-beta is upregulated in Q fever endocarditis, IL-IO might be considered as a marker of disease relapses and might be instrumental in monitoring the efficiency of the treatment.