Search

Acinetobacter baumannii is a Gram-negative opportunistic bacterium responsible for nosocomial and community-acquired infections. This pathogen is globally disseminated and associated with high levels of antibiotic resistance, which makes it an important threat to human health. Recently, new evidence showed that several A. baumannii isolates can survive and proliferate within eukaryotic professional and/or nonprofessional phagocytic cells, with in vivo consequences. This review provides updated information and describes the tools that A. baumannii possesses to adhere, colonize, and replicate in host cells. Additionally, we emphasize the high genetic and phenotypic heterogeneity detected amongst A. baumannii isolates and its impact on the bacterial intracellular features. We also discuss the need for standardized methods to characterize this pathogen robustly and consequently consider some strains as facultative intracellular bacteria. Acinetobacter baumannii is a problematic pathogen resistant to (i) antibiotics, (ii) environmental stresses such as desiccation, (iii) hospital disinfectants, and (iv) first-line immune-system components such as human serum and phagocytic cells. Several A. baumannii isolates can invade, persist, and even use different eukaryotic (professional and nonprofessional phagocytic) host cells as proliferation niches, pointing towards facultative intracellular abilities. Critical steps of intracellular trafficking and several virulence factors are identified, but more efforts to better characterize this host–pathogen interaction are still required. The intracellular behavior of A. baumannii isolates can impact environmental persistence, antibiotic treatments, and/or human infections. [ABSTRACT FROM AUTHOR]

Summary Type VI secretion systems (T6SSs) are nanomachines used for interbacterial killing and intoxication of eukaryotes. Although Vibrio cholerae is a model organism for structural studies on T6SSs, the underlying regulatory network is less understood. A recent study showed that the T6SS is part of the natural competence regulon in V. cholerae and is activated by the regulator TfoX. Here, we identify the TfoX homolog TfoY as a second activator of the T6SS. Importantly, despite inducing the same T6SS core machinery, the overall regulons differ significantly for TfoX and TfoY. We show that TfoY does not contribute to competence induction. Instead, TfoY drives the production of T6SS-dependent and T6SS-independent toxins, together with an increased motility phenotype. Hence, we conclude that V. cholerae uses its sole T6SS in response to diverse cues and for distinctive outcomes: either to kill for the prey’s DNA, leading to horizontal gene transfer, or as part of a defensive escape reaction. [ABSTRACT FROM AUTHOR]

Abstract: Brucella pathogens are responsible for brucellosis, a worldwide zoonosis. They are facultative intracellular pathogens characterized by their asymmetric division and their unipolar growth. This growth modality generates poles with specialized functions (through polar recruitment of polar adhesins or of cell cycle regulators) and progeny cells with potentially different fates. [Copyright &y& Elsevier]