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

## TL;DR

This study shows that Coxiella burnetii infects bone cells called osteoclasts and changes their behavior, which may explain chronic Q fever and its effects on bones.

## Contribution

The study identifies osteoclasts as a new host cell for Coxiella burnetii and reveals the role of the type IV secretion system in infection.

## Key findings

- Coxiella burnetii was found inside osteoclasts in a mouse model of Q fever.
- Bacterial replication in osteoclasts depends on the type IVB secretion system.
- Infection with wild-type bacteria inhibits osteoclast function, while a mutant strain enhances it.

## Abstract

Chronic Q fever is caused by persistent infection with the Gram-negative bacterium Coxiella burnetii. The mechanisms underlying this persistence remain elusive, but the presence of the bacteria in the bone marrow of C. burnetii-infected patients has been demonstrated. Therefore, we investigated the potential role of osteoclasts, the bone-resorbing cells, in harboring C. burnetii during infection. The histological analysis of bones from a murine model of Q fever revealed the presence of C. burnetii inside osteoclasts. In vitro infection assays confirmed that osteoclasts can be infected with C. burnetii and supported bacterial replication in a type IVB secretion system (T4BSS)-dependent manner. Wild-type C. burnetii infection 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 C. burnetii. 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.