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Patients with valvulopathy have the highest risk to develop infective endocarditis (IE), although the relationship between valvulopathy and IE is not clearly understood. Q fever endocarditis, an IE due to  Coxiella burnetii , is accompanied by immune impairment. Patients with valvulopathy exhibited increased levels of circulating apoptotic leukocytes, as determined by the measurement of active caspases and nucleosome determination. The binding of apoptotic cells to monocytes and macrophages, the hosts of  C. burnetii , may be responsible for the immune impairment observed in Q fever endocarditis. Apoptotic lymphocytes (AL) increased  C. burnetii  replication in monocytes and monocyte-derived macrophages in a cell-contact dependent manner, as determined by quantitative PCR and immunofluorescence. AL binding induced a M2 program in monocytes and macrophages stimulated with  C. burnetii  as determined by a cDNA chip containing 440 arrayed sequences and functional tests, but this program was in part different in monocytes and macrophages. While monocytes that had bound AL released high levels of IL-10 and IL-6, low levels of TNF and increased CD14 expression, macrophages that had bound AL released high levels of TGF-β1 and expressed mannose receptor. The neutralization of IL-10 and TGF-β1 prevented the replication of  C. burnetii  due to the binding of AL, suggesting that they were critically involved in bacterial replication. In contrast, the binding of necrotic cells to monocytes and macrophages led to  C. burnetii  killing and typical M1 polarization. Finally, interferon-γ corrected the immune deactivation induced by apoptotic cells: it prevented the replication of  C. burnetii  and re-directed monocytes and macrophages toward a M1 program, which was deleterious for  C. burnetii . We suggest that leukocyte apoptosis associated with valvulopathy may be critical for the pathogenesis of Q fever endocarditis by deactivating immune cells and creating a favorable environment for bacterial persistence.

The Uptake of Apoptotic Cells Drives Coxiella burnetii Replication and Macrophage Polarization: A Model for Q Fever Endocarditis