Abstract
Human monocytic ehrlichiosis (HME) is an emerging life-threatening tick-borne disease caused by the obligate intracellular bacterium Ehrlichia chaffeensis. HME is often presented as a nonspecific flu-like illness characterized by presence of fever, headache, malaise, and myalgia. However, in some cases the disease can evolve to a severe form, which is commonly marked by acute liver injury followed by multi-organ failure and toxic shock-like syndrome [1-3]. Macrophages and monocytes are the major target cells for Ehrlichia, although this bacterium can infect other cell types such as hepatocytes and endothelial cells [4]. In this article, we discuss how macrophages polarization to M1 or M2 phenotypes dictate the severity of ehrlichiosis and the outcome of infection. We will also discuss the potential mechanisms that regulate such polarization.
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