Efficient inactivation of intracellular bacteria in dormant amoeba spores by FeP

AbstractHost cells use several anti-bacterial pathways to defend against pathogens. Here, using a uropathogenic Escherichia coli (UPEC) infection model, we demonstrate that bacterial infection upregulates RhoB, which subsequently promotes intracellular bacteria clearance by inducing LC3 lipidation and autophagosome formation. RhoB binds with Beclin 1 through its residues at 118 to 140 and the Beclin 1 CCD domain, with RhoB Arg133 being the key binding residue. Binding of RhoB to Beclin 1 enhances the Hsp90-Beclin 1 interaction, preventing Beclin 1 degradation. RhoB also directly interacts with Hsp90, maintaining RhoB levels. UPEC infections increase RhoB, Beclin 1 and LC3 levels in bladder epithelium in vivo, whereas Beclin 1 and LC3 levels as well as UPEC clearance are substantially reduced in RhoB+/− and RhoB−/− mice upon infection. We conclude that when stimulated by UPEC infections, host cells promote UPEC clearance through the RhoB-Beclin 1-HSP90 complex, indicating RhoB may be a useful target when developing UPEC treatment strategies.

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Both viable and inactivated amoeba spores protect their intracellular bacteria from drinking water disinfection

Journal of Hazardous Materials ◽

10.1016/j.jhazmat.2021.126006 ◽

2021 ◽

Vol 417 ◽

pp. 126006

Author(s):

Zhenzhen He ◽

Luting Wang ◽

Yuexian Ge ◽

Siyi Zhang ◽

Yuehui Tian ◽

...

Keyword(s):

Drinking Water ◽

Water Disinfection ◽

Intracellular Bacteria ◽

Drinking Water Disinfection

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The growing repertoire of genetic tools for dissecting chlamydial pathogenesis

Pathogens and Disease ◽

10.1093/femspd/ftab025 ◽

2021 ◽

Author(s):

Arkaprabha Banerjee ◽

David E Nelson

Keyword(s):

Genetic Engineering ◽

Intracellular Bacteria ◽

Human Pathogens ◽

Pathogenic Potential ◽

Host Preferences ◽

Genetic Tools ◽

Obligate Intracellular ◽

Obligate Intracellular Bacteria ◽

Multiple Species

Abstract Multiple species of obligate intracellular bacteria in the genus Chlamydia are important veterinary and/or human pathogens. These pathogens all share similar biphasic developmental cycles and transition between intracellular vegetative reticulate bodies and infectious elementary forms, but vary substantially in their host preferences and pathogenic potential. A lack of tools for genetic engineering of these organisms has long been an impediment to the study of their biology and pathogenesis. However, the refinement of approaches developed in C. trachomatis over the last ten years, and adaptation of some of these approaches to other Chlamydia spp. in just the last few years, has opened exciting new possibilities for studying this ubiquitous group of important pathogens.

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The PTS Components in Klebsiella pneumoniae Affect Bacterial Capsular Polysaccharide Production and Macrophage Phagocytosis Resistance

Microorganisms ◽

10.3390/microorganisms9020335 ◽

2021 ◽

Vol 9 (2) ◽

pp. 335

Author(s):

Novaria Sari Dewi Panjaitan ◽

Yu-Tze Horng ◽

Chih-Ching Chien ◽

Hung-Chi Yang ◽

Ren-In You ◽

...

Keyword(s):

Survival Rate ◽

Klebsiella Pneumoniae ◽

Laser Scanning ◽

Bacterial Resistance ◽

Capsular Polysaccharide ◽

Laser Scanning Microscopy ◽

Confocal Laser ◽

Intracellular Bacteria ◽

Wild Type ◽

Macrophage Phagocytosis

Capsular polysaccharide (CPS) is a crucial virulence factor for Klebsiella pneumoniae infection. We demonstrated an association of CPS production with two phosphoenolpyruvate:carbohydrate phosphotransferase systems (PTSs). Deficiency of crr, encoding enzyme IIA of PTS, in K. pneumoniae enhanced the transcriptional activities of galF, wzi and gnd, which are in the cps gene cluster, leading to high CPS production. A crr mutant exhibited a higher survival rate in 1% hydrogen peroxide than the wild-type. The crr mutant showed less sensitivity to engulfment by macrophage (RAW 264.7) than the wild-type by observing the intracellular bacteria using confocal laser scanning microscopy (CLSM) and by calculating the colony-forming units (CFU) of intracellular bacteria. After long-term incubation, the survival rate of the intracellular crr mutant was higher than that of the wild-type. Deficiency of crr enhanced the transcriptional activities of etcABC which encodes another putative enzyme II complex of a PTS. Deletion of etcABC in the crr mutant reduced CPS production and the transcriptional activities of galF compared to those of the crr mutant. These results indicated that one PTS component, Crr, represses CPS production by repressing another PTS component, EtcABC, in K. pneumoniae. In addition, PTS plays a role in bacterial resistance to macrophage phagocytosis.

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