The recycling endosome and bacterial pathogens

Abstract

Summary Bacterial pathogens have developed a wide range of strategies to survive within human cells. A number of pathogens multiply in a vacuolar compartment, while others can rupture the vacuole and replicate in the host cytosol. A common theme among many bacterial pathogens is the use of specialized secretion systems to deliver effector proteins into the host cell. These effectors can manipulate the host’s membrane trafficking pathways to remodel the vacuole into a replication-permissive niche and prevent degradation. As master regulators of eukaryotic membrane traffic, Rab GTPases are principal targets of bacterial effectors. This review highlights the manipulation of Rab GTPases that regulate host recycling endocytosis by several bacterial pathogens including Chlamydia pneumoniae, Chlamydia trachomatis, Shigella flexneri, Salmonella enterica serovar Typhimurium, Uropathogenic Escherichia coli, and Legionella pneumophila. Recycling endocytosis plays key roles in a variety of cellular aspects such as nutrient uptake, immunity, cell division, migration and adhesion. Though much remains to be understood about the molecular basis and the biological relevance of bacterial pathogens exploiting Rab GTPases, current knowledge supports the notion that endocytic recycling Rab GTPases are differentially targeted to avoid degradation and support bacterial replication. Thus, future studies of the interactions between bacterial pathogens and host endocytic recycling pathways are poised to deepen our understanding of bacterial survival strategies.

Hijacking of the host cell Golgi byPlasmodiumliver stage parasites

“…hcGolgi fragmentation is certainly not unique to Plasmodium. Bacteria such as Chlamydia (Heuer et al, 2009; Rejman Lipinski et al, 2009) , Salmonella , and Legionella (Reviewed in (Allgood and Neunuebel, 2018; Brumell and Scidmore, 2007)), as well as various viruses (Reviewed in ((Ravindran et al, 2016; Spriggs et al, 2019)), and the parasite T. gondii (Romano et al, 2017) all induce hcGolgi fragmentation by mechanisms including molecular mimicry and modification of hcGolgi proteins, amongst which Golgins and Rab GTPases are common targets. In P. berghei, fragmentation becomes pronounced only from 24 h onwards corresponding with the initiation of parasite schizogony.…”

The Endosomal Recycling Pathway—At the Crossroads of the Cell

“…In the absence of intracellular survival strategies, these vacuoles would fuse with lysosomes within 15 to 30 min, which would result in the digestion of their contents. However, these bacteria inject virulence proteins into the cytoplasm of the host cell that commandeer Rab11 in order to divert the vacuoles away from the endolysosomal pathway and thus protect them from destruction [ 65 , 66 ].…”

Targeting Endosomal Recycling Pathways by Bacterial and Viral Pathogens

“…Owing to the space limitations, we are only able to cover limited aspects of this exciting field. Interested readers are referred to other recent excellent reviews that delve further into these endosomal recycling pathways, processes, and impact by pathogenic factors ( Personnic et al, 2016 ; Allgood and Neunuebel, 2018 ; Elwell and Engel, 2018 ; Siddiqa et al, 2018 ; Swart and Hilbi, 2020 ).…”