Figure 1.

Brucella invasion and intracellular trafficking in host mammalian cells. Smooth Brucella is internalized in a vacuole following interactions with host cell lipid rafts, PrPc, and SR-A. Brucella derived β-1,2-glucans act by remodeling surface vacuolar lipid-rich domains. The vacuole then fuses transiently with host cell lysosomes for replication- competent bacteria. These transient interactions lead to activation of acid-dependent genes, including type 4 secretion system. Type 4 secretion system substrate proteins are translocated to the cytosol of the host cell where they purportedly act to support trafficking and interactions with the endoplasmic reticulum in order to reach the replicative vacuole. In contrast, internalization and intracellular trafficking of rough Brucella is poorly characterized but a role for Brucella Omp22 and Omp25 has been demonstrated. The events that occur after internalization are not clear but ultimately lead to lysosomal degradation.