Interleukin-17 levels in<i>Helicobacter pylori</i>-infected gastric mucosa and pathologic sequelae of colonization

Mizuno, Tomokazu

doi:10.3748/wjg.v11.i40.6305

Cited by 87 publications

(81 citation statements)

References 44 publications

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“…Although a direct correlation with a specific pathologic marker or set of markers could not be identified, weak positive correlations were seen with RF in the serum or saliva, detectable IL-6 and IL-17 secreted in saliva, and hyposalivation (Ͻ0.1 ml/minute). While it has been reported that IL-17 may play a role in the inflammatory responses to Helicobacter pyloriinfected gastric mucosa (36), none of the study participants was tested for H pylori (data not shown).…”

Section: Resultsmentioning

confidence: 99%

Salivary gland tissue expression of interleukin‐23 and interleukin‐17 in Sjögren's syndrome: Findings in humans and mice

Nguyen

et al. 2008

Arthritis & Rheumatism

264

228

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Objective. Recently, the Th1/Th2 paradigm has been expanded by the discovery of Th17 cells, a subset of CD4؉ memory T cells characterized by their unique ability to secrete interleukin-17 (IL-17) family cytokines. Importantly, Th17 cells appear to be intimately involved in autoimmunity. We undertook the present study to investigate whether the Th17/IL-23 system is up-regulated in Sjögren's syndrome (SS).Methods. Sera, saliva, and salivary glands from C57BL/6.NOD-Aec1Aec2 mice (a model for primary SS), as well as sera, saliva, and salivary gland biopsy specimens obtained from patients with primary SS, were evaluated for IL-17 and IL-23 expression by immunohistochemistry, real-time polymerase chain reaction, and the Luminex system.Results. Immunohistochemical stainings of submandibular glands from C57BL/6.NOD-Aec1Aec2 mice and of salivary gland biopsy specimens from SS patients revealed strong positive staining for both IL-17 and IL-23 within lymphocytic foci and diffuse staining on epithelial tissues. Temporal expression of IL-17 and IL-23 in submandibular glands of C57BL/6.NODAec1Aec2 mice correlated with expression of retinoic acid-related orphan receptor ␥t, the Th17 cell master control gene. While IL-17 could not be detected in saliva from 4-20-week-old C57BL/6.NOD-Aec1Aec2 mice, this cytokine was present in the blood of mice up to age 16 weeks. This contrasted with sera and saliva from SS patients, in which IL-17 and IL-6 were present at varying levels.Conclusion. These results suggest that the Th17/ IL-23 system is up-regulated in C57BL/6.NOD-Aec1Aec2 mice and SS patients at the time of disease. A correlation between up-regulated IL-17/IL-23 expression and specific clinical manifestations of SS has yet to be identified.

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Section: Resultsmentioning

confidence: 99%

Salivary gland tissue expression of interleukin‐23 and interleukin‐17 in Sjögren's syndrome: Findings in humans and mice

Nguyen

et al. 2008

Arthritis & Rheumatism

264

228

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“…By real-time PCR and Western blotting it was shown that IL-17 up-regulation occurs at both RNA and protein levels in H pylori-infected biopsies in comparison to uninfected biopsies either with or without gastritis [13,14] . Notably, among H pylori-positive patients, the gastric mucosa at the site of ulcers contains more IL-17 than the non-ulcerated mucosa of the antrum [15] . Several observations suggest that IL-17 plays a decisive role in the neutrophil recruitment to the H pylori-infected gastric mucosa.…”

Section: Introductionmentioning

confidence: 99%

“…Infection is inversely correlated with socioeconomic (LPMC)-derived molecules. In this context, we and others have recently shown that IL-17, a key regulator of neutrophil chemotaxis, is produced in excess in H pylori-infected stomach [13][14][15] . By real-time PCR and Western blotting it was shown that IL-17 up-regulation occurs at both RNA and protein levels in H pylori-infected biopsies in comparison to uninfected biopsies either with or without gastritis [13,14] .…”

Section: Introductionmentioning

confidence: 99%

“…Several observations suggest that IL-17 plays a decisive role in the neutrophil recruitment to the H pylori-infected gastric mucosa. First, IL-17 levels correlate with the number of neutrophils infiltrating the Hp-infected mucosa [15] . Second, both gastric LPMC and epithelial cells express IL-17 receptors and are functionally capable of responding to IL-17 by secreting IL-8 [14][15][16] .…”

Section: Introductionmentioning

confidence: 99%

“…First, IL-17 levels correlate with the number of neutrophils infiltrating the Hp-infected mucosa [15] . Second, both gastric LPMC and epithelial cells express IL-17 receptors and are functionally capable of responding to IL-17 by secreting IL-8 [14][15][16] . Consistently, conditioned media of gastric epithelial cells stimulated with IL-17 enhance the migration of peripheral blood neutrophils, and this effect is inhibitable by a blocking anti-IL-8, but not anti-IL-17 antibody ( Figure 1) [14] .…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

Caruso¹

2007

WJG

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IL‐23‐mediated regulation of IL‐17 production in Helicobacter pylori‐infected gastric mucosa

Caruso¹,

Fina²,

Paoluzi³

et al. 2008

Eur J Immunol

147

125

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Helicobacter pylori (Hp) infection is associated with a marked infiltration of the gastric mucosa by inflammatory cells. The molecular pathways that control Hp-associated inflammatory reaction are complex, but locally induced cytokines seem to contribute to maintaining the ongoing inflammation. We have previously shown that IL-17 is over-produced in Hp-infected gastric mucosa, and that IL-17 stimulates the synthesis of IL-8, the major neutrophil chemoattractant. Factors/mechanisms that regulate IL-17 expression remain, however, unknown. In this study, we initially expanded our previous data, showing that CD4(+) and CD8(+) T cells are a source of IL-17 in Hp-infected samples. Since IL-23 enhances T cell-derived IL-17 during bacterial infections, we then assessed the role of IL-23 in controlling IL-17 expression in Hp-colonized stomach. Using real-time PCR and ELISA, IL-23 was detected in all gastric biopsies, but its expression was more pronounced in Hp-infected samples in comparison to controls. Treatment of normal gastric lamina propria mononuclear cells (LPMC) with IL-23 enhanced Stat3 activation and IL-17 secretion, and pharmacological inhibition of Stat3 prevented IL-23-driven IL-17 synthesis. Consistently, blockade of IL-23 in cultures of LPMC from Hp-infected patients reduced Stat3 activation and IL-17 production. Data show that IL-23 is overexpressed in Hp-infected gastric mucosa where it could contribute to sustaining IL-17 production.

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Interleukin-17 levels inHelicobacter pylori-infected gastric mucosa and pathologic sequelae of colonization

Abstract: IL-17 may play an important role in the inflammatory response to H pylori colonization, and may ultimately influence the outcome of H pylori-associated diseases that arise within the context of gastritis.

Cited by 87 publications

References 44 publications

Salivary gland tissue expression of interleukin‐23 and interleukin‐17 in Sjögren's syndrome: Findings in humans and mice

Salivary gland tissue expression of interleukin‐23 and interleukin‐17 in Sjögren's syndrome: Findings in humans and mice

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

IL‐23‐mediated regulation of IL‐17 production in Helicobacter pylori‐infected gastric mucosa

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