The Lectin LecB Induces Patches with Basolateral Characteristics at the Apical Membrane to Promote Pseudomonas aeruginosa Host Cell Invasion

Thuenauer, Roland; Kühn, Katja; Guo, Yubing; Kotsis, Fruzsina; Xu, Maokai; Trefzer, Axel; Altmann, S.; Wehrum, Sarah; Heshmatpour, Najmeh; Faust, Brian; Landi, Alessia; Diedrich, Britta; Dengjel, Jörn; Kuehn, E. Wolfgang; Römer, Winfried

doi:10.1128/mbio.00819-22

Cited by 3 publications

(3 citation statements)

References 51 publications

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“…The only reported effect of a bacterium on the primary cilium is a study that showed that treatment of cells with P . aeruginosa lectin LecB removed primary cilia in the context of major actin reorganization [ 41 ]. In both these cases, there was no evidence of AurA-HDAC6 pathway involvement, or that primary cilia loss was beneficial to the microbe.…”

Section: Discussionmentioning

confidence: 99%

“…The viral protein ORF10 activates the ubiquitin ligase CUL2 ZYG11B , promoting ubiquitination and degradation of IFT46, which is required for primary cilium formation and maintenance. The only reported effect of a bacterium on the primary cilium is a study that showed that treatment of cells with P. aeruginosa lectin LecB removed primary cilia in the context of major actin reorganization [41]. In both these cases, there was no evidence of AurA-H-DAC6 pathway involvement, or that primary cilia loss was beneficial to the microbe.…”

Section: Plos Pathogensmentioning

confidence: 99%

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Chlamydia trachomatis induces disassembly of the primary cilium to promote the intracellular infection

Ekka,

Gutierrez,

Johnson

et al. 2024

PLoS Pathog

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Chlamydia trachomatis is a clinically important bacterium that infects epithelial cells of the genitourinary and respiratory tracts and the eye. These differentiated cells are in a quiescent growth state and have a surface organelle called a primary cilium, but the standard Chlamydia cell culture infection model uses cycling cells that lack primary cilia. To investigate if these differences are relevant, we performed infections with host cells that have a primary cilium. We found that C. trachomatis caused progressive loss of the primary cilium that was prevented by disrupting Aurora A (AurA), HDAC6 or calmodulin, which are components of the cellular cilia disassembly pathway. Stabilization of the primary cilium by targeting this pathway caused a large reduction in infectious progeny although there were no changes in chlamydial inclusion growth, chlamydial replication or the ultrastructural appearance of dividing and infectious forms (RBs and EBs, respectively). Thus, the presence of a primary cilium interfered with the production of infectious EBs at a late step in the developmental cycle. C. trachomatis infection also induced quiescent cells to re-enter the cell cycle, as detected by EdU incorporation in S-phase, and Chlamydia-induced cilia disassembly was necessary for cell cycle re-entry. This study therefore describes a novel host-pathogen interaction in which the primary cilium limits a productive Chlamydia infection, and the bacterium counteracts this host cell defense by activating the cellular cilia disassembly pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Plos Pathogensmentioning

confidence: 99%

Chlamydia trachomatis induces disassembly of the primary cilium to promote the intracellular infection

Ekka,

Gutierrez,

Johnson

et al. 2024

PLoS Pathog

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show abstract

“…The P. aeruginosa surface lectin, LecB, was shown to bind β 1-integins causing rapid integrin endocytosis, which loosened cell-substrate adhesion, permitting P. aeruginosa to “crawl” underneath polarized cells ( 53 ). LecB was also shown to bind to fucosylated receptors at the apical plasma membrane of epithelial cells, which results in a Src-PI3K/Akt signaling cascade ultimately leading to the recruitment of caveolin-1 to the apical domain and enhanced invasion efficiency of P. aeruginosa ( 54 ).…”

Section: Bacterial Internalization Mechanisms Into Non-phagocytic Cellsmentioning

confidence: 99%

Evidence for intracellular Pseudomonas aeruginosa

Resko,

Suhi,

Thota

et al. 2024

J Bacteriol

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Pseudomonas aeruginosa is a significant cause of global morbidity and mortality. Although it is often regarded as an extracellular pathogen toward human cells, numerous investigations report its ability to survive and replicate within host cells, and additional studies demonstrate specific mechanisms enabling it to adopt an intracellular lifestyle. This ability of P. aeruginosa remains less well-investigated than that of other intracellular bacteria, although it is currently gaining attention. If intracellular bacteria are not killed after entering host cells, they may instead receive protection from immune recognition and experience reduced exposure to antibiotic therapy, among additional potential advantages shared with other facultative intracellular pathogens. For this review, we compiled studies that observe intracellular P. aeruginosa across strains, cell types, and experimental systems in vitro , as well as contextualize these findings with the few studies that report similar observations in vivo . We also seek to address key findings that drove the perception that P. aeruginosa remains extracellular in order to reconcile what is currently understood about intracellular pathogenesis and highlight open questions regarding its contribution to disease.

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Manipulation of host cell plasma membranes by intracellular bacterial pathogens

Kostow¹,

Welch²

2023

Current Opinion in Microbiology

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The Lectin LecB Induces Patches with Basolateral Characteristics at the Apical Membrane to Promote Pseudomonas aeruginosa Host Cell Invasion

Cited by 3 publications

References 51 publications

Chlamydia trachomatis induces disassembly of the primary cilium to promote the intracellular infection

Chlamydia trachomatis induces disassembly of the primary cilium to promote the intracellular infection

Evidence for intracellular Pseudomonas aeruginosa

Manipulation of host cell plasma membranes by intracellular bacterial pathogens

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