Analysis of the type IV secretion system-dependent cell motility of Helicobacter pylori-infected epithelial cells

2004 ◽  
Vol 322 (3) ◽  
pp. 860-866 ◽  
Author(s):  
Laila Al-Ghoul ◽  
Silja Wessler ◽  
Tanja Hundertmark ◽  
Sabine Krüger ◽  
Wolfgang Fischer ◽  
...  
2020 ◽  
Vol 158 (6) ◽  
pp. S-185
Author(s):  
Lydia Wroblewski ◽  
Alberto Delgado ◽  
Maria B. Piazuelo ◽  
Judith Romero-Gallo ◽  
Robert J. Coffey ◽  
...  

2014 ◽  
Vol 82 (8) ◽  
pp. 3457-3470 ◽  
Author(s):  
Elizabeth M. Johnson ◽  
Jennifer A. Gaddy ◽  
Bradley J. Voss ◽  
Ewa E. Hennig ◽  
Timothy L. Cover

ABSTRACTHelicobacter pyloricauses numerous alterations in gastric epithelial cells through processes that are dependent on activity of thecagtype IV secretion system (T4SS). Filamentous structures termed “pili” have been visualized at the interface betweenH. pyloriand gastric epithelial cells, and previous studies suggested that pilus formation is dependent on the presence of thecagpathogenicity island (PAI). Thus far, there has been relatively little effort to identify specific genes that are required for pilus formation, and the role of pili in T4SS function is unclear. In this study, we selected 7 genes in thecagPAI that are known to be required for T4SS function and investigated whether these genes were required for pilus formation.cagT,cagX,cagV,cagM, andcag3mutants were defective in both T4SS function and pilus formation; complemented mutants regained T4SS function and the capacity for pilus formation.cagYandcagCmutants were defective in T4SS function but retained the capacity for pilus formation. These results define a set ofcagPAI genes that are required for both pilus biogenesis and T4SS function and reveal that these processes can be uncoupled in specific mutant strains.


2008 ◽  
Vol 76 (7) ◽  
pp. 3293-3303 ◽  
Author(s):  
Chih-Ho Lai ◽  
Yun-Chieh Chang ◽  
Shin-Yi Du ◽  
Hung-Jung Wang ◽  
Chun-Hsien Kuo ◽  
...  

ABSTRACT Infection with Helicobacter pylori cagA-positive strains is associated with gastritis, ulcerations, and gastric cancer. CagA is translocated into infected epithelial cells by a type IV secretion system and can be tyrosine phosphorylated, inducing signal transduction and motogenic responses in epithelial cells. Cellular cholesterol, a vital component of the membrane, contributes to membrane dynamics and functions and is important in VacA intoxication and phagocyte evasion during H. pylori infection. In this investigation, we showed that cholesterol extraction by methyl-β-cyclodextrin reduced the level of CagA translocation and phosphorylation. Confocal microscope visualization revealed that a significant portion of translocated CagA was colocalized with the raft marker GM1 and c-Src during infection. Moreover, GM1 was rapidly recruited into sites of bacterial attachment by live-cell imaging analysis. CagA and VacA were cofractionated with detergent-resistant membranes (DRMs), suggesting that the distribution of CagA and VacA is associated with rafts in infected cells. Upon cholesterol depletion, the distribution shifted to non-DRMs. Accordingly, the CagA-induced hummingbird phenotype and interleukin-8 induction were blocked by cholesterol depletion. Raft-disrupting agents did not influence bacterial adherence but did significantly reduce internalization activity in AGS cells. Together, these results suggest that delivery of CagA into epithelial cells by the bacterial type IV secretion system is mediated in a cholesterol-dependent manner.


2001 ◽  
Vol 120 (5) ◽  
pp. A652-A653
Author(s):  
Y HIRATA ◽  
S MAEDA ◽  
Y MITUNO ◽  
M AKANUMA ◽  
T KAWABE ◽  
...  

2019 ◽  
Vol 156 (6) ◽  
pp. S-171-S-172 ◽  
Author(s):  
Lydia Wroblewski ◽  
Eunyoung Choi ◽  
Christine Petersen ◽  
Alberto Delgado ◽  
M. Blanca Piazuelo ◽  
...  

ChemBioChem ◽  
2021 ◽  
Author(s):  
Jacky Lu ◽  
Kathryn Haley ◽  
Jamisha Francis ◽  
Miriam Guevara ◽  
Ryan Doster ◽  
...  

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