Circulating levels of interleukin (IL)-12 and IL-13 in Helicobacter pylori-infected patients, and their associations with bacterial CagA and VacA virulence factors

Eskandari-Nasab, Ebrahim; Sepanjnia, Adel; Moghadampour, Mehdi; Hadadi‐Fishani, Mehdi; Rezaeifar, Alireza; Asadi-Saghandi, Abolghasem; Kalani, Behrooz Sadeghi; Manshadi, Mahdi Dehghan; Pourrajab, Fatemeh; Pourmasoumi, Hossein

doi:10.3109/00365548.2012.737930

Cited by 26 publications

(16 citation statements)

References 48 publications

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“…The overall effect of the stimulation of H. pylori was consistent with previous findings [39]. The production of different cytokines could be induced by the infiltration of immunocyte (such as T lymphocytes, monocyte and neutrophils) into diseased tissues [40–42]. A previous study found that H. pylori mainly activated the expression of IL-8 in gastric tissue by the expression of CagA [43].…”

Section: Discussionsupporting

confidence: 87%

Effect ofHelicobacter pyloriinfection on chronic periodontitis by the change of microecology and inflammation

Zhang

et al. 2016

Oncotarget

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Helicobacter pylori (H. pylori), a pathogen inducing peptic disease, is recently found to be binding to the progress of periodontitis. Most previous studies are case-controlled, and they investigate the risk of H. pylori infection in disease the development of while few studies evaluate the correlation between H. pylori and periodontal pathogens. Therefore, we investigated the correlation between H. pylori infection with periodontal parameters, periodontal pathogens and inflammation. The results indicated that patients with H. pylori showed significantly higher probing depth and attachment loss than those without (p < 0.05). Among 28 subgingival plaque samples from 14 patients, the frequencies of Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum and Treponema denticola were significantly higher with H. pylori infection than those without H. pylori infection (p < 0.05). However, the frequency of Aggregatibacter actinomycetemcomitans was lower (p < 0.05). Furthermore, after human acute monocytic leukemia cell line (THP-1) was stimulated with cagA-positive standard strains (cagA+ H. pylori 26695), the expression of periodontitis-related molecules Wnt5a, interleukin 8 (IL-8), interleukin 6 (IL-6) and interferon gamma (IFN-γ) significantly increased (p < 0.05). Conversely, the expression of tumor necrosis factor alpha (TNF-α) was almost stable. Meanwhile, cagA+ H. pylori promoted significantly higher expression of IL-8 and Wnt5a than isogenic cagA mutants strains (cagA− H. pylori 26695) did. Taken together, our data suggested that H. pylori might promote the growth of some periodontal pathogens and aggravate the progress of chronic periodontitis.

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Section: Discussionsupporting

confidence: 87%

Effect ofHelicobacter pyloriinfection on chronic periodontitis by the change of microecology and inflammation

Zhang

et al. 2016

Oncotarget

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“…Development of the gastric H. pylori infection is caused by the infiltration of T lymphocytes, plasma cells, mononuclear phagocytes, and neutrophils into the gastric mucosa; the production of various pro-inflammatory cytokines (like IL-1β, IL-6, IL-8, IL-12, and TNF-α); and chemokines from the above immune cells (20)(21)(22)(23). IL-8 plays a major role in gastric mucosal damage induced by H. pylori with its activator and chemotactic effects (24,25).…”

Section: Discussionmentioning

confidence: 99%

The cytokine response in THP-1 (monocyte) and HL-60 (neutrophil-differentiated) cells infected with different genotypes of Helicobacter pylori strains

Caliskan

Sayi-Yazgan²,

Tokman³

et al. 2015

Turk J Gastroenterol

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Background/Aims: Helicobacter pylori (H. pylori) is a microaerophilic bacterium related with peptic ulcer and gastric cancer. Its virulence factors include cytotoxin-associated gene A (CagA) and vacuolating cytotoxin gene A (VacA) proteins. Cytokine release inducted by H. pylori colonization has an important role in pathogenesis of H. pylori. The severity of gastric pathologies depends on the H. pylori genotypes found in different geographical regions. We aimed to determine the relationship between different H. pylori genotypes and their effects on the cytokine release levels. Materials and Methods: ureC, cagA, vacAs1/s2, vacAm1/m2, and blood group antigen-binding adhesion protein A2 (babA2) virulence related genes were investigated in 21 H. pylori strains. Genotyping of 21 strains were made due to the presence of cagA, vacAs1/s2, vacAm1/m2, and babA2 genes. The H. pylori strains were cultured together with THP-1 and neutrophil-differentiated Human promyelocytic leukemia cells (HL-60) cells. The levels of cytokines interleukin (IL)-1β, IL-6, IL-8, IL-12, tumor necrosis factor-alpha (TNF-α), and IL-10 in these cells were measured after co-culturing with H. pylori strains. Results: The following five different genotypes were detected: Genotype1: cagA and vacAs1m2; Genotype2: cagA and vacAs1m1; Genotype3: cagA, vacAs1m2, and babA2; Genotype4: vacAs2m2; and Genotype5: cagA and vacAs2m2. All these genotypes significantly induced the levels of IL-1β, IL-6, IL-8, IL 10, and TNF-α in THP-1 cells. Genotype 5 caused higher amounts of IL-1β, IL-6, TNF-α, and IL-10, whereas genotype 1 induced the highest levels of IL-8. In neutrophil-differentiated HL-60 cells, genotype 4 increased IL-6 levels and genotype 3 and 4 elevated IL-8 levels significantly. Conclusion: These results suggested that cytokine response of the host varies depending on the specific immune response of the host against different H. pylori strains.

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“…H. pylori , and particularly HP‐NAP, has a strong ability to induce IL‐12 and IL‐23 production in human monocytes, dendritic cells, and neutrophils . It has been shown that circulating levels of IL‐12 and IL‐18 are increased in patients infected by Cag‐positive/Vac‐positive strains . Moreover, Rezaeifar et al.…”

Section: Innate Immunitymentioning

confidence: 99%

Immunity, Inflammation, and Vaccines for Helicobacter pylori

D’Elios

Czinn

2014

Helicobacter

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Helicobacter pylori colonizes mucosa, activates Toll-like and Nod-like receptors, and usually elicits a gastric T-helper 1/17 (Th1/Th17) type of immune response. Among several bacterial factors, the secreted peptidyl prolyl cis, trans-isomerase of H. pylori represents a key factor driving Th17 inflammation. A complex and fascinating balance between H. pylori and host factors takes part in the gastric niche and is responsible for the chronicity of the infection. Novel insights into the innate and adaptive responses against H. pylori, dealing with gastric epithelial cells, cytokines, and immune evasion have been elucidated over the past year and are discussed for the development of an effective vaccine.Helicobacter pylori chronically infects the stomach of more than half of the human population and represents the major cause of gastroduodenal diseases. However, only 15-20% of H. pylori-infected patients develop severe pathologies, such as gastric cancer, gastric B-cell lymphoma, peptic ulcer, or gastric autoimmunity, during their lifetime. This fact suggests that the type of immunity elicited by H. pylori may represent an important factor that is able to influence the outcome of the infection toward protection, evasion, or pathology. Here, we present an overview of the major findings on the host response to H. pylori published over the past year.

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Circulating levels of interleukin (IL)-12 and IL-13 in Helicobacter pylori-infected patients, and their associations with bacterial CagA and VacA virulence factors

Cited by 26 publications

References 48 publications

Effect ofHelicobacter pyloriinfection on chronic periodontitis by the change of microecology and inflammation

Effect ofHelicobacter pyloriinfection on chronic periodontitis by the change of microecology and inflammation

The cytokine response in THP-1 (monocyte) and HL-60 (neutrophil-differentiated) cells infected with different genotypes of Helicobacter pylori strains

Immunity, Inflammation, and Vaccines for Helicobacter pylori

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