Decreased circulating interleukin-33 concentration in Helicobacter pylori-infected patients with peptic ulcer: Evaluation of its association with a cytokine gene polymorphism, gender of patients and bacterial virulence factor CagA

Bassagh, Arezoo; Jafarzadeh, Abdollah; Kazemi-Pour, Nadia; Nemati, Maryam; Aminizadeh, Najmeh; Larussa, Tiziana; Ghazizadeh, Motahareh; Abasi, Mehdi Hayatbakhsh; Mirkamandar, Ehsan

doi:10.1016/j.micpath.2019.103708

Cited by 3 publications

(3 citation statements)

References 47 publications

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“…Cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) proteins have been identified as virulence factors displayed by H. pylori and are considered the main virulence factors that cause the development of severe gastric lesions and immune responses (Yong et al, 2015;Sinnett et al, 2016). CagA-positive H. pylori have been found to induce more severe mucosal damages and inflammatory responses (Bassagh et al, 2019). Increased gastric VacA expression during H. pylori infection is associated with inflammation and premalignant pathology (Sinnett et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

CD103 Promotes the Pro-inflammatory Response of Gastric Resident CD4+ T Cell in Helicobacter pylori-Positive Gastritis

Chen

Ming

Lao

et al. 2020

Front. Cell. Infect. Microbiol.

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CD103 is considered as a surface marker for the resident immune cells. However, little is known about the intrinsic function of CD103 in infection and inflammation. In this study, we found that CD103 was highly expressed in CD4 + T cells of the gastric mucosa from patients with H. pylori-positive gastritis. Mucosal resident CD103 + CD4 + T cells exhibited an increase in the CD45RO + CCR7 − effector memory phenotype and high expression of the chemokine receptors CXCR3 and CCR9 compared with those in CD103 − CD4 + T cells. An In vitro coculture study demonstrated that H. pylori-specific antigen CagA/VacA-primed dendritic cells (DCs) induced proliferation and IFN-γ, TNF as well as IL-17 production by CD103 + CD4 + T cells from patients with H. pylori-positive gastritis, while blocking CD103 with a neutralizing antibody reduced proliferation and IFN-γ, TNF, and IL-17 production by CD103 + CD4 + T cells cocultured with DCs. Moreover, immunoprecipitation revealed that CD103 interacted with TCR α/β and CD3ζ, and activation of CD103 enhanced the phosphorylation of ZAP70 induced by the TCR signal. Finally, increased T-bet and Blimp1 levels were also observed in CD103 + CD4 + T cells, and activating CD103 increased T-bet and Blimp1 expression in CD4 + T cells. Our results explored the intrinsic function of CD103 in gastric T cells from patients with H. pylori-positive gastritis, which may provide a therapeutic target for the treatment of gastritis.

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Section: Introductionmentioning

confidence: 99%

CD103 Promotes the Pro-inflammatory Response of Gastric Resident CD4+ T Cell in Helicobacter pylori-Positive Gastritis

Chen

Ming

Lao

et al. 2020

Front. Cell. Infect. Microbiol.

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“…So far, this represents the first protocol of a systematic review focused exclusively on susceptibility to H. pylori infection, without any association with the resulting pathologies of the host-parasite interaction. The occurrence of this infection in the population reaches around 90% in developing countries, making the study highly relevant in these communities, and less than 40% in developed countries (González et al, 2014;Bassagh et al, 2019). Investigating susceptibility is important to understand this imbalance in the host-parasite relationship.…”

Section: Discussionmentioning

confidence: 99%

Research Article Association between host genetic polymorphisms and susceptibility to <i>Helicobacter</i> <i>pylori</i> infection: a systematic review protocol

Santos,

Maciel,

Ramos

et al. 2023

Genet. Mol. Res.

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H.C.O. Santos et al. 2 susceptibility to H. pylori infection. This protocol has been registered in the International Prospective Register of Systematic Reviews with number CRD42023409085. It was prepared in accordance with the guidelines of the Joanna Briggs Institute for systematic review protocols concerning etiology and risk. The literature searches will be conducted in electronic bibliographic databases. The selection process will be conducted in pairs, using a double-blind format, and any discrepancies will be resolved by a third reviewer. After selection, the relevant data will be extracted and recorded in a designated form. This is designed to find genetic polymorphisms associated with specific clinical outcomes, potentially helping provide valuable insights for precision medicine, allowing the development of personalized and effective therapeutic approaches in patient treatment.

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“…Moreover, the following polymorphisms in various cytokines have been linked with an increased risk of PUD: TNF-a À1031 and À863 single nucleotide polymorphisms (SNPs) [11], low levels of interleukin-35 and interleukin-33,high levels of interleukin-37 with genetic variation at SNP rs3761548 (AA genotype and A allele) in the forkhead box p3 (FOXP3) gene, rs1929992 (GG genotype and G allele) in the intron 3 region of the IL-33 gene, and the rs3811047 and rs2723176 SNPs (genotype GG and allele G, genotypes CC and allele C, respectively) on chromosome 2q13 respectively with CagA-positive HP infection [12][13][14]. In these studies, certain limitations in the expression of a genetic region, determinations of regulatory T (Treg) cell frequency and the measurements of other cytokines were not investigated.…”

Section: Introductionmentioning

confidence: 99%

The role of toll-like receptors in peptic ulcer disease

Jin

Nepal

Gao

2021

Immunological Medicine

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Helicobacter pylori (HP) is the primary etiologic factor that induces events in the immune system that lead to peptic ulcers. Toll-like receptors (TLRs) are an important part of the innate immune system, as they play pivotal roles in pathogen-associated molecular pattern (PAMP) recognition of HP as well host-associated damage-associated molecular patterns (DAMPs). Recent advancements such as COX-2 production, LPS recognition through TLR2, CagL, and CagY protein of HP activating TLR5, TLR9 activation via type IV secretion system (T4SS) using DNA transfer, TLR polymorphisms, their adaptor molecules, cytokines, and other factors play a significant role in PUD. Thus, some novel PUD treatments including Chuyou Yuyang granules, function by TLR4/NF-jB signaling pathway suppression and TNF-a and IL-18 inhibition also rely on TLR signaling. Similarly glycyrrhetinic acid (GA) treatment activates TLR-4 in Ana-1 cells not via TRIF, but via MYD88 expression, which is significantly upregulated to cure PUD. Therefore, understanding TLR signaling complexity and its resultant immune modulation after host-pathogen interactions is pivotal to drug and vaccine development for other diseases as well including cancer and recent pandemic COVID-19. In this review, we summarize the TLRs and HP interaction; its pathophysiology-related signaling pathways, polymorphisms, and pharmaceutical approaches toward PUD.

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Decreased circulating interleukin-33 concentration in Helicobacter pylori-infected patients with peptic ulcer: Evaluation of its association with a cytokine gene polymorphism, gender of patients and bacterial virulence factor CagA

Cited by 3 publications

References 47 publications

CD103 Promotes the Pro-inflammatory Response of Gastric Resident CD4+ T Cell in Helicobacter pylori-Positive Gastritis

CD103 Promotes the Pro-inflammatory Response of Gastric Resident CD4+ T Cell in Helicobacter pylori-Positive Gastritis

Research Article Association between host genetic polymorphisms and susceptibility to <i>Helicobacter</i> <i>pylori</i> infection: a systematic review protocol

The role of toll-like receptors in peptic ulcer disease

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