Erratum: Helicobacter pylori exploits human CEACAMs via HopQ for adherence and translocation of CagA

Königer, Verena; Holsten, Lea; Harrison, Ute; Busch, Benjamin; Loell, Eva; Zhao, Qi; Bonsor, Daniel A.; Roth, Alexandra; Tchoupa, Arnaud Kengmo; Smith, Stella Ifeanyi; Mueller, Susanna; Sundberg, Eric J.; Zimmermann, Wolfgang; Fischer, Wolfgang; Hauck, Christof R.; Haas, Rainer

doi:10.1038/nmicrobiol.2016.233

Cited by 17 publications

(21 citation statements)

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“…The results are representative of three independent experiments depends on HopQ as recently reported(Javaheri et al, 2016;Koniger et al, 2016). Adherent cells (a) AGS, (b) MKN45, (c) Caco2, and (d) AZ-521 cells were infected with the indicated H. pylori wild-type and ΔvacA mutant strains for 9 hr and subjected to phase-contrast microscopy.…”

mentioning

confidence: 78%

“…First, we investigated if AZ-521 cells express integrin-β 1 and CEACAMs, which are required for CagA translocation (Javaheri et al, 2016;Jimenez-Soto et al, 2009;Koniger et al, 2016;Kwok et al, 2007). Total cell lysates of strains P12, P310, and P420 as well as their corresponding ΔvacA mutants were subjected to western blotting using α-VacA, α-CagA, α-UreB, α-GGT, and α-FlaA antibodies.…”

Section: Az-521 Cells Express Integrin-β 1 But Not Ceacamsmentioning

confidence: 99%

“…Once this first contact is achieved, the T4SS can establish binding to numerous host cell surface factors such as integrin receptors and phosphatidylserine to assist the delivery of CagA, possibly in lipid rafts (cholesterol-rich microdomains) in the focal adhesions (Backert et al, 2015;Hayashi et al, 2012;Kwok et al, 2007;Lai et al, 2008;Posselt, Backert, & Wessler, 2013;Tegtmeyer, Wessler, et al, 2017). A fourth group of factors, the CEACAM receptors and their bacterial ligand HopQ, came into play just recently and are also required for full T4SS function (Bonsor et al, 2018;Javaheri et al, 2016;Koniger et al, 2016;Moonens et al, 2018). A fourth group of factors, the CEACAM receptors and their bacterial ligand HopQ, came into play just recently and are also required for full T4SS function (Bonsor et al, 2018;Javaheri et al, 2016;Koniger et al, 2016;Moonens et al, 2018).…”

Section: Expression Of Ceacam1 and Ceacam5 Enhances Caga-mediated Tmentioning

confidence: 99%

“…The blots show that all these known virulence factors are expressed in similar amounts and that the ΔvacA mutants only lack VacA expression as expected gastrointestinal epithelial cell line. First, we investigated if AZ-521 cells express integrin-β 1 and CEACAMs, which are required for CagA translocation (Javaheri et al, 2016;Jimenez-Soto et al, 2009;Koniger et al, 2016;Kwok et al, 2007). For this purpose, AZ-521 cells with growing confluency were harvested after 2, 4, or 6 days of culturing and subjected to western blotting.…”

Section: Az-521 Cells Express Integrin-β 1 But Not Ceacamsmentioning

confidence: 99%

“…Moreover, recent studies have demonstrated that H. pylori also targets various receptors of the carcinoembryonic antigen-related cell adhesion molecule (CEACAM) family via the exposed outer membrane adhesin HopQ, permitting bacterial adhesion and delivery of CagA (Bonsor et al, 2018;Javaheri et al, 2016;Koniger et al, 2016;Moonens et al, 2018). The HopQ-CEACAM binding is glycanindependent and triggers CEACAM1-dependent host cell signalling, which is required for T4SS functionality, bacterial colonisation, and gastric pathology.…”

Section: Introductionmentioning

confidence: 99%

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Expression of CEACAM1 or CEACAM5 in AZ-521 cells restores the type IV secretion deficiency for translocation of CagA byHelicobacter pylori

Tegtmeyer

Harrer

Schmitt

et al. 2018

Cellular Microbiology

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Helicobacter pylori represents an important pathogen involved in diseases ranging from gastritis, peptic ulceration, to gastric malignancies. Prominent virulence factors comprise the vacuolating cytotoxin VacA and the cytotoxin-associated genes pathogenicity island (cagPAI)-encoded type IV secretion system (T4SS). The T4SS effector protein CagA can be translocated into AGS and other gastric epithelial cells followed by phosphorylation through c-Src and c-Abl tyrosin kinases to hijack signalling networks. The duodenal cell line AZ-521 has been recently introduced as novel model system to investigate CagA delivery and phosphorylation in a VacA-dependent fashion. In contrast, we discovered that AZ-521 cells display a T4SS incompetence phenotype for CagA injection, which represents the first reported gastrointestinal cell line with a remarkable T4SS defect. We proposed that this deficiency may be due to an imbalanced coexpression of T4SS receptor integrin-β 1 or carcinoembryonic antigenrelated cell adhesion molecules (CEACAMs), which were described recently as novel H. pylori receptors. We demonstrate that AZ-521 cells readily express integrin-β 1 , but overexpression of integrin-β 1 constructs did not restore the T4SS defect. We further show that AZ-521 cells lack the expression of CEACAMs. We demonstrate that genetic introduction of either CEACAM1 or CEACAM5, but not CEACAM6, in AZ-521 cells is sufficient to permit injection and phosphorylation of CagA by H. pylori to degrees observed in the AGS cell model. Expression of CEACAM1 or CEACAM5 in infected AZ-521 cells was also accompanied by tyrosine dephosphorylation of the cytoskeletal proteins vinculin and cortactin, a hallmark of H. pylori-infected AGS cells.Our results suggest the existence of an integrin-β 1and CEACAM1-or CEACAM5dependent T4SS delivery pathway for CagA, which is clearly independent of VacA.The presence of two essential host protein receptors during infection with H. pylori represents a unique feature in the bacterial T4SS world. Further detailed investigation of these T4SS functions will help to better understand infection strategies by bacterial pathogens.

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mentioning

confidence: 78%

Section: Az-521 Cells Express Integrin-β 1 But Not Ceacamsmentioning

confidence: 99%

Section: Expression Of Ceacam1 and Ceacam5 Enhances Caga-mediated Tmentioning

confidence: 99%

Section: Az-521 Cells Express Integrin-β 1 But Not Ceacamsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Expression of CEACAM1 or CEACAM5 in AZ-521 cells restores the type IV secretion deficiency for translocation of CagA byHelicobacter pylori

Tegtmeyer

Harrer

Schmitt

et al. 2018

Cellular Microbiology

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Early Detection of Helicobacter Pylori Bacteria in Complex Samples

Jaradat

Al‐Hamry

Ibbini

et al. 2021

Smart Sensors, Measurement and Instrumentation

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Virulence of Helicobacter pylori outer membrane proteins: an updated review

Soyfoo

et al. 2020

Eur J Clin Microbiol Infect Dis

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Helicobacter pylori (H. pylori) infection is associated with some gastric diseases, such as gastritis, peptic ulcer, and gastric cancer. CagA and VacA are known virulence factors of H. pylori, which play a vital role in severe clinical outcomes. Additionally, the expression of outer membrane proteins (OMPs) helps H. pylori attach to gastric epithelial cells at the primary stage and increases the virulence of H. pylori. In this review, we have summarized the paralogs of H. pylori OMPs, their genomic loci, and the different receptors of OMPs identified so far. We focused on five OMPs, BabA (HopS), SabA (HopP), OipA (HopH), HopQ, and HopZ, and one family of OMPs: Hom. We highlight the coexpression of OMPs with other virulence factors and their relationship with clinical outcomes. In conclusion, OMPs are closely related to the pathogenic processes of adhesion, colonization, persistent infection, and severe clinical consequences. They are potential targets for the prevention and treatment of H. pylori-related diseases.

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Erratum: Helicobacter pylori exploits human CEACAMs via HopQ for adherence and translocation of CagA

Cited by 17 publications

References 0 publications

Expression of CEACAM1 or CEACAM5 in AZ-521 cells restores the type IV secretion deficiency for translocation of CagA byHelicobacter pylori

Expression of CEACAM1 or CEACAM5 in AZ-521 cells restores the type IV secretion deficiency for translocation of CagA byHelicobacter pylori

Early Detection of Helicobacter Pylori Bacteria in Complex Samples

Virulence of Helicobacter pylori outer membrane proteins: an updated review

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