The biological functions of IL-17 in different clinical expressions of Helicobacter pylori-infection

Bagheri, Nader; Azadegan‐Dehkordi, Fatemeh; Shirzad, Hedayatollah; Rafieian-Kopaei, Mahmoud; Rahimian, Ghorbanali; Razavi, Alireza

doi:10.1016/j.micpath.2015.03.010

Cited by 71 publications

(52 citation statements)

References 67 publications

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“…Research has shown it to be associated with the host inflammatory response and an increased risk for clinical outcomes. 12 Van Doorn et al have shown an association between lower eradication efficacy and H.pylori strains missing the CagA gene, while Scholte et al did not find this relation.…”

Section: Discussionmentioning

confidence: 95%

The influence of vitamin D deficiency on eradication rates of Helicobacter pylori

Yıldırım¹,

Yıldırım²,

Seçkin³

et al. 2017

Adv Clin Exp Med

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Section: Discussionmentioning

confidence: 95%

The influence of vitamin D deficiency on eradication rates of Helicobacter pylori

Yıldırım¹,

Yıldırım²,

Seçkin³

et al. 2017

Adv Clin Exp Med

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“…Helicobacter pylori infection is associated with gastritis and considerable infiltration of neutrophils, monocytes, and lymphocytes into the gastric mucosa, which contribute to maintaining and expanding local inflammation. Activation and migration of these inflammatory cells into the gastric mucosa is related to increased production of pro-inflammatory cytokines, which are believed to contribute in maintaining the gastric inflammation and causing epithelial cell damage [2–4]. The risk of different clinical expression of H. pylori infection is thought to rely on interaction between the host genetic factors and bacterial factors.…”

Section: Introductionmentioning

confidence: 99%

Clinical immunology Mucosal interleukin-21 mRNA expression level is high in patients with Helicobacter pylori and is associated with the severity of gastritis

Bagheri

Azadegan‐Dehkordi

Shirzad

et al. 2015

cejoi

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Helicobacter pylori (H. pylori) infection is associated with gastritis and marked infiltration of the gastric mucosa by several cytokines secreting inflammatory cells. Different clinical forms of the infection may reflect distinctive patterns of cytokine expression. Interleukin (IL)-17, IL-21, IL-22, and IL-23 have been reported to be involved in H. pylori-induced gastric mucosal inflammation, but the details and relationship to different patterns of inflammation and virulence factors remain unclear. The present study was launched to analyse IL-6 expression in H. pylori-infected and uninfected gastric patients and to investigate its correlation with chronic gastritis among H. pylori-infected patients. Total RNA was extracted from the gastric antrum biopsies of 48 H. pylori-infected patients and 38 H. pylori uninfected patients. Mucosal IL-21 mRNA expression level in H. pylori-infected and uninfected gastric biopsy was determined by real-time PCR. The presence of vacA (vacuolating cytotoxin A) and cagA (cytotoxin associated gene A) virulence factors were evaluated using PCR. Interleukin-21 mRNA expression was significantly high in biopsies of H. pylori-infected patients compared to H. pylori uninfected patients, and the mucosal IL-21 mRNA level was positively correlated with the grade of chronic inflammation. There was no association between virulence factors and IL-21 mRNA expression. We believe that IL-21 might be involved in the pathogenesis of H. pylori and might be an index of the severity of chronic gastritis.

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“…IL-17A is the best characterized and is primarily produced by T helper type 17 (Th17) cells (10,11). Several lines of evidence suggest that IL-17A plays an important role in the pathophysiology of H. pylori-associated disease (12,13). For example, Caruso et al (14) showed that IL-17A-producing T cells were increased in H. pylori-infected gastric mucosa and that IL-17A was overexpressed.…”

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Interleukin-17C in Human Helicobacter pylori Gastritis

et al. 2017

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The interleukin-17 (IL-17) family of cytokines (IL-17A to IL-17F) is involved in many inflammatory diseases. Although IL-17A is recognized as being involved in the pathophysiology of Helicobacter pylori-associated diseases, the role of other IL-17 cytokine family members remains unclear. Microarray analysis of IL-17 family cytokines was performed in H. pylori-infected and uninfected gastric biopsy specimens. IL-17C mRNA was upregulated approximately 4.5-fold in H. pylori-infected gastric biopsy specimens. This was confirmed by quantitative reverse transcriptase PCR in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominican Republic. Immunohistochemical analysis showed that IL-17C expression in H. pylori-infected gastric biopsy specimens was predominantly localized to epithelial and chromogranin A-positive endocrine cells. IL-17C mRNA levels were also significantly greater among cagA-positive than cagA-negative H. pylori infections (P ϭ 0.012). In vitro studies confirmed an increase in IL-17C mRNA and protein levels in cells infected with cagA-positive infections compared to cells infected with either cagA-negative or cag pathogenicity island (PAI) mutant. Chemical inhibition of IB kinase (IKK), mitogen-activated protein extracellular signal-regulated kinase (MEK), and Jun N-terminal kinase (JNK) inhibited induction of IL-17C proteins in infected cells, whereas p38 inhibition had no effect on IL-17C protein secretion. In conclusion, H. pylori infection was associated with a significant increase in IL-17C expression in human gastric mucosa. The role of IL-17C in the pathogenesis of H. pyloriinduced diseases remains to be determined.

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The biological functions of IL-17 in different clinical expressions of Helicobacter pylori-infection

Cited by 71 publications

References 67 publications

The influence of vitamin D deficiency on eradication rates of Helicobacter pylori

The influence of vitamin D deficiency on eradication rates of Helicobacter pylori

Clinical immunology Mucosal interleukin-21 mRNA expression level is high in patients with Helicobacter pylori and is associated with the severity of gastritis

Interleukin-17C in Human Helicobacter pylori Gastritis

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