%0 Journal Article
%9 ACL : Articles dans des revues avec comité de lecture répertoriées par l'AERES
%A Mehraj, V.
%A Textoris, J.
%A Ben Amara, A.
%A Ghigo, E.
%A Raoult, Didier
%A Capo, C.
%A Mege, J. L.
%T Monocyte responses in the context of Q fever : from a static polarized model to a kinetic model of activation
%D 2013
%L PAR00010932
%G ENG
%J Journal of Infectious Diseases
%@ 0022-1899
%K macrophage ; microarray ; monocyte ; Q fever ; polarization
%M ISI:000324510200011
%N 6
%P 942-951
%R 10.1093/infdis/jit266
%U https://www.documentation.ird.fr/hor/PAR00010932
%V 208
%W Horizon (IRD)
%X 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.
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