Circulating T‐Cell Response to <i>Helicobacter pylori</i> Infection in Chronic Gastritis

Ren, Zhigang; Pang, Gerald; Lee, Roger; Batey, Robert; Dunkley, Margaret; Borody, Thomas J.; Clancy, Robert

doi:10.1046/j.1523-5378.2000.00021.x

Cited by 38 publications

(39 citation statements)

References 25 publications

(41 reference statements)

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“…Thus in the protective immune response to H pylori, Th1 and Th2 are needed. It must have a balance between Th1 and Th2 to achieve immune protection and to prevent tissue from damaging by serious inflammation [23] . In our study, before challenge by alive H pylori, the levels of IFN, IL-12, IL-4 and IL-10 were significantly higher in the groups with chitosan than in other groups without adjuvant, indicating that in the early stage of immune, they induce immune response to both Th1 and Th2.…”

Section: Discussionmentioning

confidence: 99%

Th immune response induced byH pylorivaccine with chitosan as adjuvant and its relation to immune protection

Xie

Zhou²,

Gong³

et al. 2007

WJG

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Section: Discussionmentioning

confidence: 99%

Th immune response induced byH pylorivaccine with chitosan as adjuvant and its relation to immune protection

Xie

Zhou²,

Gong³

et al. 2007

WJG

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“…Several studies have shown that infection with this pathogen triggers a Th1-type immune response, i.e., effector CD4 ϩ T cells producing gamma interferon (IFN-␥) but not interleukin-4 (IL-4), IL-5, or IL-13 in response to infection (2,26,38,39). However, this response does not enable the immune system to clear the infection and may instead be detrimental to tissue integrity.…”

mentioning

confidence: 99%

Helicobacter pyloriInduces Transendothelial Migration of Activated Memory T Cells

et al. 2005

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Helicobacter pylori infection is associated with pronounced infiltration of granulocytes and lymphocytes into the gastric mucosa, resulting in active chronic gastritis that may develop into duodenal ulcer disease or gastric adenocarcinoma. Infiltrating T cells play a major role in the pathology of these diseases, but the signals involved in recruitment of T cells from blood to H. pylori-infected tissues are not well understood. We therefore examined H. pylori-induced T-cell transendothelial migration (TEM). The Transwell system, employing a monolayer of human umbilical vein endothelial cells, was used as a model to study TEM. H. pylori induced a significant T-cell migration, compared to spontaneous migration. CD4؉ and CD8 ؉ T cells migrated to the same extent in response to H. pylori, whereas there was significantly larger transmigration of memory T cells compared to naive T cells. Both H. pylori culture filtrate and urease induced migration, and the presence of the H. pylori cag pathogenicity island increased TEM. T-cell TEM was mediated by LFA-1-ICAM-1 interactions in accordance with an increased ICAM-1 expression on the endothelial cells after contact with H. pylori. Migrating T cells had increased expression of activation marker CD69 and chemokine receptors CXCR3, CCR4, and CCR9. Furthermore, T cells migrating in response to H. pylori secreted Th1 but not Th2 cytokines upon stimulation. In conclusion, our data indicate that live H. pylori and its secreted products contribute to T-cell recruitment to the gastric mucosa and that the responding T cells have an activated memory Th1 phenotype.

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“…A similar mucosal response in immune mice following oral challenge with C albicans, has shown protection to include a positive paracrine loop involving IL-4 and nitric oxide (11). The data in these studies show not only a low baseline IL-4 secretion, but also an absence of the 'switch' and of the antigen-induced enhancement of cytokine secretion, which characterize an effective response to eradication (8). It is not clear whether the defective 'switch' characteristics reflect the primary defect of low IL-4 secretion or persisting bacterial colonization.…”

Section: Commentmentioning

confidence: 73%

“…Most mucosal T cells in patients infected with H pylori, secrete cytokines characteristic of a Th1 response (7). Following successful eradication, the cytokine pattern switches to one more characteristic of a balance between Th1 and Th2 cells, the so-called Th0 response (8). Mucosal cultures from patients with gastric cancer or precancer showed an extreme Th2 polarization, with high levels of IL-4 and an absence of IFN-γ (9).…”

Section: Peut-on Prévoir L'issue Du Traitement Suppressif D'helicobacmentioning

confidence: 99%

Can the Response to Eradication Therapy in Helicobacter pylori Infection be Predicted?

Clancy

Borody

Ren³

et al. 2003

Canadian Journal of Gastroenterology and Hepatology

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The failure to eradicate Helicobacter pylori infection with antibiotic therapy has become a major clinical problem, not entirely accounted for by either poor compliance or antibiotic resistance. Recognition that failed eradication is one outcome of the host-parasite relationship focuses attention on impaired host protection as a determinant of nonresponse to antibiotics. A secreted interleukin (IL)-4 whole blood assay was developed to determine whether persistent infection was contributed to by impaired cytokine responses. The blood assay was shown to correlate well with mucosal organ cultures. Significantly lower levels of IL-4 were detected in the whole blood assays in 11 subjects with failed eradication compared with subjects with successful eradication (P<0.05). This latter group underwent a Th1 to Th0 'switch', which appears to be important to successful eradication. Detection of subjects at risk for failing to eradicate infection with standard combination therapy, by virtue of low secreted L'échec du traitement suppressif des infections à Helicobacter pylori par l'antibiothérapie est devenu un problème clinique important, qu'on ne peut attribuer entièrement à un manque d'observance thérapeutique ou à la résistance aux antibiotiques. Le fait de reconnaître que l'échec de la suppression résulte de la relation hôte-parasite fait ressortir l'absence de protection adéquate de l'hôte comme facteur déterminant de non-réac-tion aux antibiotiques. Un test de dosage de l'interleukine 4 (IL-4) sur sang entier a été mis au point pour savoir si une réaction inadéquate des cytokines pouvait expliquer la persistance de l'infection. Le dosage sanguin est en étroite corrélation avec les cultures d'organes muqueux. Des taux significativement bas d'IL-4 ont été décelés chez 11 sujets chez qui la suppression avait échoué comparativement aux sujets chez qui la suppression avait porté fruit (P<0,05). Ces derniers sont passés de Th1 à Th0, ce qui semble un facteur important pour la réussite du traitement. Le repérage des patients susceptibles de ne pas réagir favorablement à la suppression de H pylori par la polythérapie usuelle à cause d'un faible taux d'IL-4 dans les cultures sur sang entier pourrait s'avérer utile sur le plan clinique.

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Circulating T‐Cell Response to Helicobacter pylori Infection in Chronic Gastritis

Cited by 38 publications

References 25 publications

Th immune response induced byH pylorivaccine with chitosan as adjuvant and its relation to immune protection

Th immune response induced byH pylorivaccine with chitosan as adjuvant and its relation to immune protection

Helicobacter pyloriInduces Transendothelial Migration of Activated Memory T Cells

Can the Response to Eradication Therapy in Helicobacter pylori Infection be Predicted?

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