Association of the CagA status of Helicobacter pylori and serum levels of interleukin (IL)‐17 and IL‐23 in duodenal ulcer patients

Abstract

OBJECTIVE:It has been reported that the cytotoxinassociated gene A (cagA+) H. pylori strains induce severe gastric mucosal inflammation. The aim of this study was to investigate the association of the virulence factor CagA with IL-17 and IL-23 serum levels in duodenal ulcer (DU) patients and H. pylori-infected asymptomatic (AS) carriers. METHODS:In total, 45 H. pylori-infected DU patients were enrolled to study: 23 tested positive for the anti-CagA antibody (anti-CagA+) and 22 tested negative for the anti-CagA antibody (anti-CagA-), 30 were AS carriers (15 were anti-CagA+ and 15 were anti-CagA-) and 15 were healthy uninfected participants (as a control group). The IL-17 and IL-23 serum levels of participants were measured by enzyme-linked immunosorbent assay method. RESULTS:The mean IL-17 levels in DU patients were significantly higher than those in AS and control groups (P < 0.001 and P < 0.0001 respectively). In the DU group, the mean IL-17 levels in participants testing positive for anti-CagA (10.84 ± 5.79 pg/mL) were significantly higher than those observed in participants testing negative for anti-CagA (7.65 ± 4.74 pg/mL; P < 0.05). The mean IL-23 levels in the DU and AS groups were significantly higher than in the control group (P < 0.02 and P < 0.03 respectively) but were not significantly different in participants testing positive and negative for anti-CagA. CONCLUSION:These results showed higher IL-17 and IL-23 serum levels in H. pylori-infected participants than in the control group. In the DU group the expression of IL-17 was influenced by the CagA factor.

Diminished circulating concentration of interleukin‐35 in Helicobacter pylori‐infected patients with peptic ulcer: Its association with FOXP3 gene polymorphism, bacterial virulence factor CagA, and gender of patients

“…A close relationship was also indicated between H. pylori CagA + strains with PU disease and the expression of the inflammatory and pathological parameters . Higher levels of inflammatory cytokines such as TNF‐α, IL‐8, IL‐17, and IL‐18 were also indicated in H. pylori ‐infected patients, especially in those infected with CagA + strain of bacteria IL‐18 …”

<I>HELICOBACTER PYLORI</I> INFECTION IN NEVER-SMOKING MALE PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND ITS RELATION TO LUNG FUNCTION

“…It is believed that the release of proinflammatory cytokines, e.g., Interleukin-1 (IL-1), IL-8, IL-17, IL-23 and Tumor Necrosis Factor-ά (TNF-ά), stimulated by H. pylori infection plays a role in the chronic inflammation of bronchi (Roussos et al, 2006;Jafarzadeh et al, 2009;Cornwell et al, 2010). Moreover, serum levels of these cytokines normalize following eradication therapy of H. pylori (Kountouras et al, 2000).…”

Toll-like receptor 2: An important immunomodulatory molecule during Helicobacter pylori infection

“…In addition, CagApositive strains of H. pylori were more potent than CagA-negative strains in TLR2-induced cytokine secretion from macrophages, indicating the contribution of CagA or other PAI-associated genes in TLR2-related cytokine production [57]. The results of a number of studies show that the expression of pro-inflammatory cytokines and mediators were higher in infected subjects with CagA-positive strains than CagA-negative strains [13,14,58,59]. Experimentally, it has been also demonstrated that the IL-6 and IL-1β secretion by bone-marrow derived macrophages in response to H. pylori is mediated by TLR2 [31].…”