| Summary: | The <i>Brucella</i> species is the causative agent of brucellosis in humans and animals. So far, brucellosis has caused considerable economic losses and serious public health threats. Furthermore, <i>Brucella</i> is classified as a category B bioterrorism agent. Although the mortality of brucellosis is low, the pathogens are persistent in mammalian hosts and result in chronic infection. <i>Brucella</i> is a facultative intracellular bacterium; hence, it has to invade different professional and non-professional phagocytes through the host phagocytosis mechanism to establish its lifecycle. The phagocytosis of <i>Brucella</i> into the host cells undergoes several phases including <i>Brucella</i> detection, formation of <i>Brucella</i>-containing vacuoles, and <i>Brucella</i> survival via intracellular growth or being killed by host-specific bactericidal activities. Different host surface receptors contribute effectively to recognize <i>Brucella</i> including non-opsonic receptors (toll-like receptors and scavenger receptor A) or opsonic receptors (Fc receptors and complement system receptors). <i>Brucella</i> lacks classical virulence factors such as exotoxin, spores, cytolysins, exoenzymes, virulence plasmid, and capsules. However, once internalized, <i>Brucella</i> expresses various virulence factors to avoid phagolysosome fusion, bypass harsh environments, and establish a replicative niche. This review provides general and updated information regarding <i>Brucella</i> phagocytosis mediated by pathogen-host interactions and their intracellular survival in host cells.
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