Chronic Exposure to<i>Helicobacter pylori</i>Impairs Dendritic Cell Function and Inhibits Th1 Development

Mitchell, Peter; Germain, Conrad; Fiori, Pier Luigi; Khamri, Wafa; Foster, Graham R.; Ghosh, Subrata; Lechler, Robert I.; Bamford, Kathleen B.; Lombardi, Giovanna

doi:10.1128/iai.00228-06

Cited by 83 publications

(86 citation statements)

References 55 publications

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“…RNA transcripts for both p40 and p19 subunits were also up-regulated in biopsies from H pyloriinfected patients, indicating that IL-23 is regulated at the transcriptional level in this condition [13] . These results confirm and expand on data of previous studies showing that H pylori enhances IL-23 secretion by monocyte-derived DC [27] , and that H pylori neutrophil-activating protein (H pylori-NAP), a member of a broad super-family of ferritin-like proteins, induces IL-23 production by neutrophils and monocytes [28,29] . Functional studies also revealed that [13] .…”

Section: Il-23 Controls Il-17 Production In the Human Gastric Mucosasupporting

confidence: 81%

Emerging role of IL-23/IL-17 axis inH pylori-associated pathology

Caruso¹

2007

WJG

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Section: Il-23 Controls Il-17 Production In the Human Gastric Mucosasupporting

confidence: 81%

Emerging role of IL-23/IL-17 axis inH pylori-associated pathology

Caruso¹

2007

WJG

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“…Interestingly, H. pylori organisms, when added to MDDC, do not directly stimulate IL-12 production [38] but instead induce IL-23. The lack of IL-12 secretion was suggested to contribute to the lack of adequate T cell responses and subsequent lack of clearance of H. pylori.…”

Section: Discussionmentioning

confidence: 99%

“…Another microorganism that affects DC is the mucosal pathogen Helicobacter pylori which stimulates MDDC, but prolonged stimulation reduces DC antigen-presenting function, possibly due to DC exhaustion after prolonged exposure [38]. Interestingly, H. pylori organisms, when added to MDDC, do not directly stimulate IL-12 production [38] but instead induce IL-23.…”

Section: Discussionmentioning

confidence: 99%

Dendritic cell activation and maturation induced by mucosal fluid from women with bacterial vaginosis

John

Martinson

Simões

et al. 2007

Clinical Immunology

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Dendritic cells (DC) at mucosal surfaces mature when exposed to "danger" signals such as LPS. Bacterial vaginosis (BV) is a prevalent alteration of the vaginal bacterial flora associated with preterm childbirth and increased risk for HIV acquisition. We examined the effect of mucosal fluid from women with BV or healthy flora on DC function. IL-12, IL-23 and p40 production by monocytederived dendritic cells (MDDC) were all induced by BV samples. Activation/maturation markers HLA-DR, CD40, and CD83 on MDDC incubated with BV CVL were also induced. BV CVL also decreased the endocytic ability of MDDC and increased proliferation of T-cells in allogeneic MLR. Plasmacytoid dendritic cell (pDC) CD86 expression was induced by BV CVL. Healthy flora CVL had little effect in any of the tests. This study suggests that BV, but not healthy flora, affects local dendritic cell function in vivo suggesting a mechanism through which BV affects mucosal immunity.

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“…Direct evidence for this comes from a study that compared H. pylori-induced IL-12 secretion by monocyte-derived DCs following short-term and sustained stimulation with fixed H. pylori. Whereas short-term stimulation induced DC maturation and strong IL-12 responses, sustained stimulation significantly impaired DC function and reduced the secretion of IL-12 (72). Lending further support to the notion that H. pylori skews the Th1/Th2 balance by reducing IL-12 secretion, Kao et al (66) recently identified a nonproteinaceous factor in sonicates of H. pylori that has the ability to prevent IL-12 secretion by DC in vitro, indicating H. pylori may act to actively suppress DC function, as opposed to causing exhaustion through chronic stimulation.…”

Section: Yersinia Enterocolitica Inhibits Ag Presentation By Dcsmentioning

confidence: 99%

Different Bacterial Pathogens, Different Strategies, Yet the Aim Is the Same: Evasion of Intestinal Dendritic Cell Recognition

Bedoui

Kupz

Wijburg

et al. 2010

The Journal of Immunology

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Given the central role of intestinal dendritic cells (DCs) in the regulation of gut immune responses, it is not surprising that several bacterial pathogens have evolved strategies to prevent or bypass recognition by DCs. In this article, we will review recent findings on the interaction between intestinal DCs and prototypical bacterial pathogens, such as Salmonella, Yersinia, or Helicobacter. We will discuss the different approaches with which these pathogens seek to evade DC recognition and subsequent T cell activation. These diverse strategies span to include mounting irrelevant immune responses, inhibition of Ag presentation by DCs, and stretch as far as to manipulate the Th1/Th2 balance of CD4+ T cells in the bacteria’s favor.

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Chronic Exposure toHelicobacter pyloriImpairs Dendritic Cell Function and Inhibits Th1 Development

Cited by 83 publications

References 55 publications

Emerging role of IL-23/IL-17 axis inH pylori-associated pathology

Emerging role of IL-23/IL-17 axis inH pylori-associated pathology

Dendritic cell activation and maturation induced by mucosal fluid from women with bacterial vaginosis

Different Bacterial Pathogens, Different Strategies, Yet the Aim Is the Same: Evasion of Intestinal Dendritic Cell Recognition

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