Background: H. pylori infection is associated with gastritis and marked infiltration of the gastric mucosa
by inflammatory cells secreting of several cytokines that contribute to maintain and expand the local
inflammation. Different clinical expressions of the infection may reflect different patterns of cytokine
expression. Interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-17, IL-23, and IL-18 have been
reported to be involved in H. pylori-induced gastric mucosal inflammation, but the details and relation to
different patterns of inflammation remain unclear.
Materials and Methods: Analysis of IL-18 RNA transcripts was performed by real-time PCR. Total
RNA was extracted from gastric biopsies of 56 H. pylori-infected patients, 50 H. pylori-negative patients
with gastritis, by biozol reagent according to the manufacturer's instructions. CDNA was synthesized from
1 mg of total RNA using First Strand cDNA Synthesis Kit (fermentas) and 3 μL cDNA was amplified by
PCR using the 2x Rotor-Gene Probe PCR Master Mix (QIAGEN) and specific primers for each cytokine
and β-actin.
Results: IL-18 mRNA expression was significantly increased in biopsies of H. pylori-infected patients
compared to H. pylori-uninfected individuals.
Conclusion: IL-18 may play an important role in the inflammatory response and promoting gastric Th1
responses to H. pylori colonization, and may ultimately influence the outcome of H. pylori-associated
diseases that arise within the context of gastritis.
The molecular pathways that control Helicobacter pylori (Hp)-associated inflammatory reaction are complex, but locally induced cytokines and virulence factors seem to have a major role in maintaining the ongoing inflammation. Therefore this study was aimed to evaluate the association of the virulence factors of Hp and gastric mucosal interleukin-17/23 mRNA expression in dyspeptic patients. Mucosal IL-17 and IL-23 mRNA expression in H. pylori infected and non-infected gastric biopsies were determined by real-time RT-PCR. Virulence factors, vac-A and cag-A were evaluated using PCR. There was no significant difference in mucosal IL-17 and IL-23 mRNA expression between H. pylori infected and non-infected patients. Their expression in mucosa did not correlate with chronic gastritis and chronic active gastritis. IL-17 and IL-23 mRNA expression in mucosa of patients with vacA m1 were significantly higher than those observed in patients with vacA m2. The severity of polymorphonuclear infiltration and chronic active gastritis was higher in cag-A positive than cag-A negative patients. H. pylori infections carrying the vacA m1 allele have higher IL-17 and IL-23 mRNA and the current study suggests that the virulence factor vacA allele's m1 are important for the severe gastric inflammation.
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.
زمینه و هدف: اینترلوکین های 17 و 23 در دفاع بر علیه برخی عفونتهای مخاطی دستگاه گوارش نقش دارند و IL-17 باعث جذب نوتروفیل ها به محل عفونت شده و در ایجاد التهاب نقش دارد. مطالعه حاضر میزان بیان mRNA سیتوکاین های IL-17و IL-23در دو گروه بیماران گاستریتی با عفونت هلیکوباکترپیلوری و فاقد عفونت را به وسیله روش کمی Real-Time PCR بررسی میکند. روش بررسی: در این مطالعه مورد- شاهدی، از 58 بیمار دارای گاستریت با عفونت هلیکوباکترپیلوری و 50 بیمار مبتلا به گاستریت که فاقد عفونت بودند، توسط آندوسکوپی بیوپسی تهیه شد. بعد از استخراجmRNA و تبدیل آن به cDNA، میزان بیانmRNA مربوط به IL-17و IL-23در نمونهها توسط Real-Time PCR اندازه گیری شد و بیان سایتوکاین ها در دو گروه آلوده و غیر آلوده با استفاده از تست Mann–Whitney مورد آنالیز قرار گرفت. یافتهها: ارتباط معنیداری بین میزان بیانIL-17 mRNA در افراد دارای گاستریت با عفونت هلیکوباکترپیلوری و افراد دارای گاستریت فاقد عفونت دیده نشد (941/0P=). همچنین ارتباط بین میزان بیان mRNA IL-23در بیماران دارای گاستریت با عفونت هلیکوباکترپیلوری و بیماران دارای گاستریت فاقد عفونت معنی دار نبود (076/0 P=). نتیجهگیری: نتایج این مطالعه نشان داد که میزان بیان mRNA سیتوکاین های IL-17و IL-23در بیماران دارای گاستریت با عفونت هلیکوباکترپیلوری در مقایسه با بیماران گاستریتی بدون عفونت بالاتر نمیباشد و در نتیجه ارتباط معنی داری بین دو گروه مورد مطالعه در این استان وجود ندارد؛ لذا می طلبد تا نقش دقیق سایتوکاین های دیگر درگیر در بروز بیماری گاستریت جهت تعیین پیش آگهی و ارزیابی برنامه های درمانی بیشتر مشخص شود.
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