Mehraj V., Textoris J., Ben Amara A., Ghigo E., Raoult Didier, Capo C., Mege J. L. (2013). Monocyte responses in the context of Q fever : from a static polarized model to a kinetic model of activation. Journal of Infectious Diseases, 208 (6), p. 942-951. ISSN 0022-1899.
Titre du document
Monocyte responses in the context of Q fever : from a static polarized model to a kinetic model of activation
Mehraj V., Textoris J., Ben Amara A., Ghigo E., Raoult Didier, Capo C., Mege J. L.
Source
Journal of Infectious Diseases, 2013,
208 (6), p. 942-951 ISSN 0022-1899
Background. Q fever is caused by Coxiella burnetii, a bacterium that persists in M2-polarized macrophages. We wondered whether the concept of M1/M2 polarization is applicable to Q fever patients. Methods. Monocytes from healthy controls were cultured with IFN-gamma and IL-4, agonists of M1 and M2 macrophages, respectively, and their gene expression was assessed using whole-genome microarrays. Selected biomarkers were assessed in blood from Q fever patients by real-time reverse transcription polymerase chain reaction (RT-PCR). Results. Monocytes exhibited early (6-hour) patterns of activation specific to IFN-gamma or IL-4 and a late (18-hour) pattern of common activation. Because these responses were not reducible to M1/M2 polarization, we selected biomarkers and tested their relevance in Q fever patients. The early genes NLRC5, RTP4, and RHOH, which were modulated in response to IFN-gamma, were up-regulated in patients with acute Q fever, and the expression levels of the late genes ALOX15, CLECSF1, CCL13, and CCL23 were specifically increased in patients with Q fever endocarditis. The RHOH and ALOX15 genes were associated with the activity of acute Q fever and Q fever endocarditis, respectively. Conclusions. Our results show that the kinetic model of monocyte activation enables a dynamic approach for the evaluation of Q fever patients.
