High Concentrations of Serum Soluble E-Cadherin in Patients With Q Fever

Cadherins switching is a hallmark of neoplasic processes. The E-cadherin (E-cad) subtype is one of the surface molecules regulating cell-to-cell adhesion. After its cleavage by sheddases, a soluble fragment (sE-cad) is released that has been identified as a pro-carcinogenic inflammatory signal in several bacteria-induced cancers. Recently we reported that Q fever, a disease due to infection, can be complicated by occurrence of non-Hodgkin lymphoma (NHL). Therefore, we studied E-cad switching in Q fever. The sE-cad levels were found increased in the sera of acute and persistent Q fever patients, whereas they remained at the baseline in controls groups of healthy donors, people cured of Q fever, patients suffering from unrelated inflammatory diseases, and past Q fever patients who developed NHL. These results indicate that sE-cad can be considered as a new biomarker of infection rather than a marker of NHL-associated to Q fever. We wondered if changes in sE-cad reflected variations in the gene transcription. The expression of E-cad mRNA and its intracellular ligand β-catenin was down-regulated in peripheral blood mononuclear cells (PBMCs) of patients with either acute or persistent forms of Q fever. Indeed, a lower cell-surface expression of E-cad was measured in a minority (<5%) subpopulation of HLADR/CD16 monocytes from patients with acute Q fever. However, a very strong increase in E-cad expression was observed on more than 30% of the HLADR/CD16 monocytes of persistent Q fever patients, a cell subpopulation known to be a target for in humans. An experimental infection of healthy donors' PBMCs with , was performed to directly evaluate the link between interaction with PBMCs and their E-cad expression. A significant increase in the percentage of HLADR/CD16 monocytes expressing E-cad was measured after PBMCs had been incubated for 8 h with Nine Mile strain. Altogether, these data demonstrate that severely impairs the E-cad expression in circulating cells of Q fever patients.