Interaction of microbial pathogens with host exocytic pathways

Abstract

Many microbial pathogens co-opt or perturb host membrane trafficking pathways. This review covers recent examples in which microbes interact with host exocytosis, the fusion of intracellular vesicles with the plasma membrane. The bacterial pathogens Listeria monocytogenes and Staphylococcus aureus subvert recycling endosomal pathways of exocytosis in order to induce their entry into human cells. By contrast, entry of the protozoan pathogen Trypanosoma cruzi or the virus adenovirus into host cells involves exploitation of lysosomal exocytosis. Toxins produced by Bacillus anthracis or Vibrio cholerae interfere with exocytosis pathways mediated by the GTPase Rab11 and the exocyst complex. By doing so, anthrax or cholera toxins impair recycling of cadherins to cell-cell junctions and disrupt the barrier properties of endothelial cells or intestinal epithelial cells, respectively. Uropathogenic Escherichia coli (UPEC) is expelled from bladder epithelial cells through two different exocytic routes that involve sensing of bacteria in vacuoles by host Toll-like receptor 4 (TLR4) or monitoring of the pH of lysosomes harbouring UPEC. The TLR4 pathway is mediated by multiple Rab GTPases and the exocyst, whereas the other pathway involves exocytosis of lysosomes. Expulsion of UPEC through these pathways is thought to benefit the host.

The Host Scaffolding Protein Filamin A and the Exocyst Complex Control Exocytosis during InlB-Mediated Entry of Listeria monocytogenes

“…Like Listeria sp. strain EGD, the bacteria Salmonella enterica serovar Typhimurium and Staphylococcus aureus exploit the exocyst complex in order to gain entry into human cells (45)(46)(47). An interesting question for future research is whether subversion of exocytosis through the exocyst is a general strategy used for internalization by bacterial pathogens.…”

Helicobacter pylori release from yeast as a vesicle‐encased or free bacterium

“…Similarly, release of free Legionella pneumophila 39 and mycobacteria 40 from unharmed ameba host has been reported. In addition to packaging of bacteria in a membranous compartment, free exit appears to be another peaceful strategy that enables bacteria to leave the host cell without destroying it 11 …”

“…Lytic escape involves bacterial release from host cell through destroying cell and vacuolar membrane by lipases, proteases, and pore‐forming proteins 10 . However, in nonlytic strategy intracellular bacteria escape from the host cell without destroying it, either as free bacteria or encased by host membranes 10,11 …”

Activation of the macroautophagy pathway byYersinia enterocoliticapromotes intracellular multiplication and egress of yersiniae from epithelial cells

“…Experimental verification of this hypothesis and its potential implication in Yersinia pathogenesis has yet to be specified. But, it is interesting to note that Rab11 (Connor et al, 2018), VAMP3, and VAMP7 (Ligeon et al, 2014), playing roles in autophagy and being recruited to YCVs, are also important regulatory elements of the exocytic machinery (Amaya, Fader, & Colombo, 2015;Ireton, Van Ngo, & Bhalla, 2018). These molecules may consequently not only play a role in controlling the intracellular fate of Yersinia, but also in dictating the release of yersiniae from infected cells.…”

“…The externalisation of amphisomal contents is suggested to be an alternative debris removal mechanism that counterbalances insufficient elimination through the lysosomal pathway (Xu et al, 2018). But, it is interesting to note that Rab11 (Connor et al, 2018), VAMP3, and VAMP7 (Ligeon et al, 2014), playing roles in autophagy and being recruited to YCVs, are also important regulatory elements of the exocytic machinery (Amaya, Fader, & Colombo, 2015;Ireton, Van Ngo, & Bhalla, 2018). Experimental verification of this hypothesis and its potential implication in Yersinia pathogenesis has yet to be specified.…”