Eric Ghigo

Q fever is a disease caused by Coxiella burnetii, an obligate intracellular bacterium. Acute Q fever is characterized by efficient immune response, w

Q fever is a disease caused by Coxiella burnetii, an obligate intracellular bacterium. Acute Q fever is spontaneously resolutive and is characterized

Intracellular pathogens have developed different strategies to survive within host cells. For example, these pathogens might interfere with the biogenesis of phagolysosomes, thereby forming replicative vacuoles. Although the complex mechanisms used by pathogens to hijack the biogenesis of phagolysosomes have been elucidated in naive leukocytes, the role of leukocyte activation in this process has not yet been investigated. Leukocytes are known to be activated by cytokines, and several reports have demonstrated that several cytokines modulate the endocytic pathway and thereby, affect phagosome biogenesis. These observations provide molecular evidence that endocytosis can be regulated by the immune environment. In this review, we highlight the effect of leukocyte activation by cytokines on the endocytic pathway and on phagosome biogenesis. We briefly describe the mechanism of phagolysosome formation before focusing on the strategies used by two bacterial pathogens, Coxiella burnetii and Mycobacterium tuberculosis, to hijack phagolysosome biogenesis. Finally, we emphasize the effect of leukocyte activation on the endocytic pathway and on phagolysosome formation, which has not been highlighted to date.

Viruses must enter host cells to deliver their genetic material and accessory proteins. Endocytosis offers to viruses the opportunity to enter host cells. However, endocytosis is a complex phenomenon that includes different mechanisms, clathrin-mediated endocytosis, caveolin-mediated endocytosis, macropinocytosis, and phagocytosis. Here, I describe the ways used by different viruses to exploit these endocytic pathways.

Coxiella burnetii, the agent of Q fever, is an obligate intracellular bacterium that is considered a potential biological weapon of category B. C. burnetii survives within myeloid cells by subverting receptor‐mediated phagocytosis and preventing phagosome maturation. The intracellular fate of C. burnetii also depends on the functional state of myeloid cells. This review describes the mechanisms used by C. burnetii to circumvent uptake and trafficking events, and the role of cytokines on C. burnetii survival in myeloid cells.