infects osteoclasts and alters their differentiation and function in a type IV secretion system-dependent manner.

Abstract

Chronic Q fever is caused by persistent infection with the Gram-negative bacterium. The mechanisms underlying this persistence remain elusive, but the presence of the bacteria in the bone marrow of-infected patients has been demonstrated. Therefore, we investigated the potential role of osteoclasts, the bone-resorbing cells, in harboringduring infection. The histological analysis of bones from a murine model of Q fever revealed the presence ofinside osteoclasts.infection assays confirmed that osteoclasts can be infected withand supported bacterial replication in a type IVB secretion system (T4BSS)-dependent manner. Wild-typeinfection inhibited osteoclast differentiation and bone-resorbing activity, while the T4BSS mutant enhanced the differentiation and bone-degrading function of osteoclasts. Taken together, our findings identify osteoclasts as a potential host cell for. This opens new perspectives on the mechanisms that may underlie chronic Q fever as well as questioning the putative consequences on bone biology in chronically affected patients.