Helicobacter pylori vacA and cagA genotype diversity and interferon gamma expression in patients with chronic gastritis and patients with gastric cancer

Martínez‐Carrillo, Dinorah Nashely; Atrisco-Morales, Josefina; Hernández-Pando, Rogelio; Reyes-Navarrete, Salomón; Betancourt-Linares, Reyes; Carmen, Iván Cruz-del; Aguiar, Berenice Illades; Román-Román, Adolfo; Fernández‐Tilapa, Gloria

doi:10.1016/j.rgmxen.2014.12.001

Cited by 10 publications

(7 citation statements)

References 34 publications

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“…In addition, a decreased diversity in the individual human microbiome has been associated to higher probabilities of developing an array of diseases, including obesity and diabetes (17, 85, 86). However, only some Helicobacter strains carry virulence genes, commonly associated to the acquisition of pathogenicity islands, including disease-linked genes, such as CagA and VacA which encode for cytotoxins (55, 87–89). …”

Section: Potential Pathogens or Ancient Symbionts?mentioning

confidence: 99%

From Evolutionary Advantage to Disease Agents: Forensic Reevaluation of Host-Microbe Interactions and Pathogenicity

2017

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As the “human microbiome era” continues, there is an increasing awareness of our resident microbiota and its indispensable role in our increased fitness as holobionts. However, the host-microbe relationship is not so clearly defined for some human symbionts. Here we discuss examples of “accidental pathogens”, meaning previously non-pathogenic and/or environmental microbes thought to have inadvertently experienced an evolutionary shift towards pathogenicity. For instance, symbionts such as Helicobacter pylori and JC Polyomavirus have been shown to accompany humans since prehistoric times and are still abundant in extant populations as part of the microbiome. And yet, the relationship between a subgroup of these microbes and their human hosts seems to have changed with time, and they have recently gained notoriety as gastrointestinal and neuropathogens, respectively. On the other hand, environmental microbes such as Legionella spp. have recently experienced a shift in host range and are now a major problem in industrialized countries as a result of artificial ecosystems. Other variables involved in this accidental phenomenon could be the apparent change or reduction in the diversity of human-associated microbiota because of modern medicine and lifestyles. All of this could result in an increased prevalence of “accidental pathogens” in the form of emerging pathogens.

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Section: Potential Pathogens or Ancient Symbionts?mentioning

confidence: 99%

From Evolutionary Advantage to Disease Agents: Forensic Reevaluation of Host-Microbe Interactions and Pathogenicity

2017

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“…Increased gastric VacA expression during H. pylori infection is associated with inflammation and premalignant pathology (Sinnett et al, 2016). IFN-γ expression in gastric biopsies varies depending on the H. pylori vacA and cagA genotype (Martinez-Carrillo et al, 2014). In particular, H. pylori infection promotes the Th17 immune response through the virulence factor CagA (Lina et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

CD103 Promotes the Pro-inflammatory Response of Gastric Resident CD4+ T Cell in Helicobacter pylori-Positive Gastritis

Chen

Ming

Lao

et al. 2020

Front. Cell. Infect. Microbiol.

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CD103 is considered as a surface marker for the resident immune cells. However, little is known about the intrinsic function of CD103 in infection and inflammation. In this study, we found that CD103 was highly expressed in CD4 + T cells of the gastric mucosa from patients with H. pylori-positive gastritis. Mucosal resident CD103 + CD4 + T cells exhibited an increase in the CD45RO + CCR7 − effector memory phenotype and high expression of the chemokine receptors CXCR3 and CCR9 compared with those in CD103 − CD4 + T cells. An In vitro coculture study demonstrated that H. pylori-specific antigen CagA/VacA-primed dendritic cells (DCs) induced proliferation and IFN-γ, TNF as well as IL-17 production by CD103 + CD4 + T cells from patients with H. pylori-positive gastritis, while blocking CD103 with a neutralizing antibody reduced proliferation and IFN-γ, TNF, and IL-17 production by CD103 + CD4 + T cells cocultured with DCs. Moreover, immunoprecipitation revealed that CD103 interacted with TCR α/β and CD3ζ, and activation of CD103 enhanced the phosphorylation of ZAP70 induced by the TCR signal. Finally, increased T-bet and Blimp1 levels were also observed in CD103 + CD4 + T cells, and activating CD103 increased T-bet and Blimp1 expression in CD4 + T cells. Our results explored the intrinsic function of CD103 in gastric T cells from patients with H. pylori-positive gastritis, which may provide a therapeutic target for the treatment of gastritis.

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“…In this study, the most frequent genotype was vacA s1m1/cagA+, in both the antrum and corpus. Other studies performed in southern Mexico reported 71.1% and 69.7% [ 30 , 31 ]; furthermore, by gastric pathology, the prevalence of this genotype was 70.7% in chronic gastritis, 57.9% in gastric ulcers, and 81.3% in gastric cancer [ 32 ]. These findings suggest that the vacA s1m1/cagA+ genotype predominates in the Mexican population.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Virulence Factors and Clarithromycin Resistance-Associated Mutations in Mexican Patients

et al. 2023

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Persistent infection with Helicobacter pylori (H. pylori) is an important factor in gastric diseases. The vacA and cagA virulence factors of H. pylori contribute to the development of these diseases. Triple therapy containing clarithromycin has been used to eradicate this infection. Unfortunately, resistance to this antibiotic is the primary cause of treatment failure. This study aimed to determine the prevalence of clarithromycin resistance-associated mutations and to assess the relationship between virulence factors and Mexican patients infected with H. pylori. The cagA and vacA genotypes were determined by multiplex PCR. Furthermore, a qPCR was used to identify mutations of the 23S rRNA gene. This study reported a prevalence of 84.3% of H. pylori among patients with gastric diseases, and the vacA s1m1/cagA+ genotype was the most frequent (44.8%) in antrum and corpus. Analysis of the 23S rRNA gene revealed a 19.8% prevalence of clarithromycin resistance-associated mutations. The most prevalent mutations were A2143G (56%) and A2142C (25%). A significant association (p < 0.05) between the A2142G and the vacA s1m1/cagA+ genotype was detected. In conclusion, we report a high prevalence (>15%) of clarithromycin resistance-associated mutations, and we found an association between the genotypes of virulence factors and a mutation in the 23S rRNA gene.

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Helicobacter pylori vacA and cagA genotype diversity and interferon gamma expression in patients with chronic gastritis and patients with gastric cancer

Cited by 10 publications

References 34 publications

From Evolutionary Advantage to Disease Agents: Forensic Reevaluation of Host-Microbe Interactions and Pathogenicity

From Evolutionary Advantage to Disease Agents: Forensic Reevaluation of Host-Microbe Interactions and Pathogenicity

CD103 Promotes the Pro-inflammatory Response of Gastric Resident CD4+ T Cell in Helicobacter pylori-Positive Gastritis

Helicobacter pylori Virulence Factors and Clarithromycin Resistance-Associated Mutations in Mexican Patients

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