Preliminary study and bioinformatics analysis on the potential role of CagQ in type IV secretion system of H.pylori

Yao, Yizheng; Shen, Yifei; Zhu, Linqi; Ni, Ying; Wang, Hua; Shao, Shihe

doi:10.1016/j.micpath.2017.12.076

Cited by 7 publications

(5 citation statements)

References 34 publications

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“…Cagζ (Cag1), a membrane protein in T4SS, is closely associated with T4SS function, IL-8 expression induction, and CagA delivery to host cells [48]. A recent study uncovered CagQ’s role as a membrane protein in T4SS for maintaining CagA expression and CagA-induced apoptotic effects [135].…”

Section: Virulence Factors Associated With Gastric Epithelial Cellmentioning

confidence: 99%

Helicobacter pylori Virulence Factors Exploiting Gastric Colonization and its Pathogenicity

Ansari

Yamaoka

2019

Toxins

189

141

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Helicobacter pylori colonizes the gastric epithelial cells of at least half of the world’s population, and it is the strongest risk factor for developing gastric complications like chronic gastritis, ulcer diseases, and gastric cancer. To successfully colonize and establish a persistent infection, the bacteria must overcome harsh gastric conditions. H. pylori has a well-developed mechanism by which it can survive in a very acidic niche. Despite bacterial factors, gastric environmental factors and host genetic constituents together play a co-operative role for gastric pathogenicity. The virulence factors include bacterial colonization factors BabA, SabA, OipA, and HopQ, and the virulence factors necessary for gastric pathogenicity include the effector proteins like CagA, VacA, HtrA, and the outer membrane vesicles. Bacterial factors are considered more important. Here, we summarize the recent information to better understand several bacterial virulence factors and their role in the pathogenic mechanism.

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Section: Virulence Factors Associated With Gastric Epithelial Cellmentioning

confidence: 99%

Helicobacter pylori Virulence Factors Exploiting Gastric Colonization and its Pathogenicity

Ansari

Yamaoka

2019

Toxins

189

141

View full text Add to dashboard Cite

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“…Many components of T4SS or other virulence factors of H. pylori have been reported to interact with CagA or affect T4SS function. For example, in addition to CagY, other T4SS components such as CagI, CagL, and CagQ were reported to interact with CagA, 69 , 70 and to be indispensable for the formation of T4SS pilus. 76 Hansen et al 65 also identified mutations in cag PAI genes including cag5, cag10, cagA , and cagY from mouse-passaged strains which lost T4SS function.…”

Section: Discussionmentioning

confidence: 99%

Host immune response mediates changes in cagA copy number and virulence potential of Helicobacter pylori

Jang

Hansen

et al. 2022

Gut Microbes

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Helicobacter pylori is the major risk factor for gastric cancer. H. pylori harboring the type IV secretion system (T4SS) and its effector CagA encoded on the cag pathogenicity Island ( cag PAI) increases the risk. H. pylori PMSS1 has a multi- cagA genotype, modulating cagA copy number dynamically from zero to four copies. To examine the effect of the immune response on cagA copy number change, we utilized a mouse model with different immune status. PMSS1 recovered from Rag1 −/− mice, lacking functional T or B cells, retained more cagA copies. PMSS1 recovered from Il10 −/− mice, showing intense inflammation, had fewer cagA copies compared to those recovered from wild-type mice. Moreover, cagA copy number of PMSS1 recovered from wild-type and Il10 −/− mice was positively correlated with the capacity to induce IL-8 secretion at four weeks of infection. Since recombination in cagY influences T4SS function, including CagA translocation and IL-8 induction, we constructed a multiple linear regression model to predict H. pylori -induced IL-8 expression based on cagA copy number and cagY recombination status; H. pylori induces more IL-8 secretion when the strain has more cagA copies and intact cagY . This study shows that H. pylori PMSS1 in mice with less intense immune response possess higher cagA copy number than those infected in mice with more intense immune response and thus the multi- cagA genotype, along with cagY recombination, functions as an immune-sensitive regulator of H. pylori virulence.

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“…Cagζ (Cag1) has been found to be closely associated with the activity of T4SS, CagA translocation, and IL-8 expression [ 65 ]. CagQ, which is a membrane protein in T4SS, plays a key role for maintaining CagA expression and CagA-induced apoptotic effects [ 66 ]. CagE protein has been found to induce IL-8 secretion, mediating the host cell cytokine rearrangement in infected cells [ 57 ].…”

Section: Caga Translocationmentioning

confidence: 99%

Helicobacter pylori Virulence Factor Cytotoxin-Associated Gene A (CagA)-Mediated Gastric Pathogenicity

Ansari

Yamaoka

2020

IJMS

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Helicobacter pylori causes persistent infection in the gastric epithelium of more than half of the world’s population, leading to the development of severe complications such as peptic ulcer diseases, gastric cancer, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Several virulence factors, including cytotoxin-associated gene A (CagA), which is translocated into the gastric epithelium via the type 4 secretory system (T4SS), have been indicated to play a vital role in disease development. Although infection with strains harboring the East Asian type of CagA possessing the EPIYA-A, -B, and -D sequences has been found to potentiate cell proliferation and disease pathogenicity, the exact mechanism of CagA involvement in disease severity still remains to be elucidated. Therefore, we discuss the possible role of CagA in gastric pathogenicity.

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Preliminary study and bioinformatics analysis on the potential role of CagQ in type IV secretion system of H.pylori

Cited by 7 publications

References 34 publications

Helicobacter pylori Virulence Factors Exploiting Gastric Colonization and its Pathogenicity

Helicobacter pylori Virulence Factors Exploiting Gastric Colonization and its Pathogenicity

Host immune response mediates changes in cagA copy number and virulence potential of Helicobacter pylori

Helicobacter pylori Virulence Factor Cytotoxin-Associated Gene A (CagA)-Mediated Gastric Pathogenicity

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