Helicobacter pylori: Bacterial Factors and the Role of Cytokines in the Immune Response

Romero-Adrián, Tania Beatriz; Leal-Montiel, Jorymar Yoselyn; Monsalve-Castillo, Francisca; Mengual-Moreno, Edgardo; McGregor, Ernesto García; Perini, Lenis; Antúnez, Ana

doi:10.1007/s00284-009-9518-4

Cited by 37 publications

(36 citation statements)

References 148 publications

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“…TNF-␣ is a proinflammatory cytokine first associated principally with macrophages but now known to be produced by both Th1 and Th17 cells (50,51). It has been associated with inflammation due to H. pylori (10,16), although its essential nature has been questioned (52). Elucidation of the role of T cell-derived TNF-␣ in H. pylori gastritis awaits further experimentation.…”

Section: Fig 10 Gastric Engraftment Of Cd4mentioning

confidence: 99%

Complex T Cell Interactions Contribute to Helicobacter pylori Gastritis in Mice

et al. 2013

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Disease due to the gastric pathogen Helicobacter pylori varies in severity from asymptomatic to peptic ulcer disease and cancer. Accumulating evidence suggests that one source of this variation is an abnormal host response. The goal of this study was to use a mouse model of H. pylori gastritis to investigate the roles of regulatory T cells (Treg) as well as proinflammatory T cells (Th1 and Th17) in gastritis, gastric T cell engraftment, and gastric cytokine production. Our results support published data indicating that severe gastritis in T cell recipient mice is due to failure of Treg engraftment, that Treg ameliorate gastritis, and that the proinflammatory response is attributable to interactions between several cell subsets and cytokines. We confirmed that gamma interferon (IFN-␥) is essential for induction of gastritis but showed that IFN-␥-producing CD4 T cells are not necessary. Interleukin 17A (IL-17A) also contributed to gastritis, but to a lesser extent than IFN-␥. Tumor necrosis factor alpha (TNF-␣) and IL-17F were also elevated in association with disease. These results indicate that while H. pylori-specific CD4 ؉ T cells and IFN-␥ are both essential for induction of gastritis due to H. pylori, IFN-␥ production by T cells is not essential. It is likely that other proinflammatory cytokines, such as IL-17F and TNF-␣, shown to be elevated in this model, also contribute to the induction of disease. We suggest that gastritis due to H. pylori is associated with loss of immunoregulation and alteration of several cytokines and cell subsets and cannot be attributed to a single immune pathway.

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Section: Fig 10 Gastric Engraftment Of Cd4mentioning

confidence: 99%

Complex T Cell Interactions Contribute to Helicobacter pylori Gastritis in Mice

et al. 2013

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“…VacA s2-m2 strains are rarely associated with the development of peptic ulcer and gastric cancer (32) . Helicobacter pylori strains have been divided into two groups: type I (cag+/s1m1 VacA) that causes ulceration and cancer, and type II (cag-/s2m2 VacA) that induces less inflammation and tissue damage (26) . Since considerable geographic diversity in the prevalence of H. pylori virulence factors has been reported, the objective of the present study was to investigate the presence of H. pylori infection and the frequency of association of different bacterial genotypes with gastrointestinal diseases in 554 patients seen at a referral hospital in the Metropolitan Region of Belém, Pará, Brazil, as well as their association with different histopathological findings.…”

Section: Helicobacter Pylori Infection In Patients With Different Gasmentioning

confidence: 99%

“…Although most hosts remain asymptomatic, others develop peptic or duodenal ulcers, gastric adenocarcinoma and lymphomas, especially mucosa-associated lymphoid tissue (MALT) lymphoma (26) . The mechanism whereby the bacterium produces different pathological manifestations in the stomach and duodenum are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Helicobacter Pylori Infection in Patients With Different Gastrointestinal Diseases From Northern Brazil

Vinagre

Queiroz

Júnior³

et al. 2015

Arq. Gastroenterol.

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-Background -The mechanisms whereby Helicobacter pylori produces different pathological manifestations in the stomach and duodenum are not fully understood. Considering the geographic diversity in the prevalence of virulence factors of this microorganism and their association with the development of different diseases, the search for pathogenicity markers such as CagA and VacA alleles by molecular techniques has intensified. Objectives -To investigate the presence of H. pylori infection and the frequency of different genotypes of this bacterium in patients with gastrointestinal diseases from Northern Brazil, and to establish their association with the histopathological findings. Methods -In a prospective study, samples were collected from 554 patients with different gastrointestinal diseases (gastritis, duodenal ulcer, gastric ulcer, and gastric cancer) seen at a referral hospital attending the entire State of Pará, located in the metropolitan region of Belém. Data such as gender and age obtained with an epidemiological questionnaire were analyzed. The presence of H. pylori and the bacterial genotype were investigated by PCR. Gastric biopsies were assessed histologically. Results -The prevalence of H. pylori infection was 91%. Infection was more frequent among patients with gastric ulcer and gastric cancer. In these groups, there was a predominance of men and older patients when compared to the other two groups studied. The predominant bacterial genotype was s1m1cagA+, which was more frequent among patients with gastric ulcer, duodenal ulcer and gastric cancer. A significant association was observed between s1m1cagA+ strains and a higher degree of inflammation, neutrophil activity and development of intestinal metaplasia. Conclusion -The present study demonstrates a high incidence of H. pylori infection in the patients analyzed, especially among those with gastric ulcer and gastric cancer. Virulent s1m-1cagA+ strains predominated and were associated with more severe lesions. HEADINGS -Helicobacter pylori. Helicobacter infections. Gastrointestinal diseases. Genotype.

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“…For example, VacA alters the function of T lymphocytes, B cells, macrophages, and mast cells (8)(9)(10)(11) and HP-NAP acts on neutrophils, mast cells, and monocytes (12,13) For many years, studies have been conducted involving the subset of T cells and cytokines in different physiological and pathological clinical entities (14)(15)(16)(17)(18)(19)(20)(21)(22). In H. pylori infection all investigations indicate the predominance of the Th1 response (14,21,23). However, other cellular phenotypes such as Th2, Th17 and Treg that secrete inmunomodulate cytokines may participate (21).…”

Section: Introductionmentioning

confidence: 99%

“…However, other cellular phenotypes such as Th2, Th17 and Treg that secrete inmunomodulate cytokines may participate (21). In the setting of H. pylori infection, multiple cytokines in the gastric mucosa (including TNF, IFN-γ, IL-1β, IL-6, IL-8, and IL-18) are predicted to have proinflammatory effects, whereas IL-10 and TGF-β are cytokines that may limit the inflammatory response (21). Early studies suggest that IL-2 is specifically required for the development and maintenance of nTregs (24).…”

Section: Introductionmentioning

confidence: 99%

<italic>Helicobacter pylori </italic>Infection: Regulatory T Cells and Their Participation in the Immune Response

Romero-Adrián

Leal-Montiel

2013

Jundishapur J Microbiol

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A B S T R A C THelicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the human stomach and affects more than half of the global human population. This microorganism shows variations in its geographical distribution and causes chronic gastritis, peptic ulcer, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma. The development of these clinical entities depends on the bacterial strain and its virulence, the host genetic predisposition, immunological response, concurrent infections and infestations.

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Helicobacter pylori: Bacterial Factors and the Role of Cytokines in the Immune Response

Cited by 37 publications

References 148 publications

Complex T Cell Interactions Contribute to Helicobacter pylori Gastritis in Mice

Complex T Cell Interactions Contribute to Helicobacter pylori Gastritis in Mice

Helicobacter Pylori Infection in Patients With Different Gastrointestinal Diseases From Northern Brazil

<italic>Helicobacter pylori </italic>Infection: Regulatory T Cells and Their Participation in the Immune Response

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