CIRCULATING CYTOKINES AND GASTRIN LEVELS IN ASYMPTOMATIC SUBJECTS INFECTED BYHELICOBACTER PYLORI (H. PYLORI)

Abstract

The pathophysiology of hypergastrinemia in H. pylori infection has been largely investigated and different reports clearly show that the infected antrum has a marked inflammatory response with a suggestive local production of cytokines. Notwithstanding, a few data are available on the circulating levels of cytokines and gastrin in the asymptomatic people carrying H. pylori infection. Thus, aim of the study was to evaluate circulating proinflammatory cytokines [Interleukin (IL)-8, Interleukin (IL)-10, Interferon (IFN)-gamma, and Tumor Necrosis Factor (TNF)-alpha] and gastrin levels in H. pylori positive asymptomatic subjects vs. H. pylori negative ones. To this end, thirty healthy volunteers with no digestive symptoms or systemic disease were enrolled and H. pylori infection was identified by a 13C-urea breath test. Plasma levels of gastrin were determined using the RIA kit whereas IL-8, TNF-alpha, IL-10, and IFN-gamma levels in serum were measured with a solid-phase ELISA. Fifteen infected people showed significantly higher gastrin and TNF-alpha levels than uninfected subjects. On the contrary, IL-8 levels were significantly higher in the uninfected subjects than in H. pylori positive ones (P < 0.0422). IFN-gamma and IL-10 circulating levels were not affected by H. pylori presence, being not significantly different in the two groups.

High Seroprevalence of <i>Helicobacter pylori</i> in Chronic Bronchitis among Chinese Population

“…The increased prevalence of CagA positive strains in our study population further supports this hypothesis. It is well known that these virulent strains and particular those CagA positive strains, stimulate the release of a variety of proinflammatory cytokines, including IL-1, IL-8 and TNF-α (Perri et al 1999;Russo et al 2001). Moreover, eradication of H. pylori leads to normalization of serum cytokines levels (Kountouras et al 2000).…”

“…It is well known that H. pylori and particularly those strains bearing the cytotoxin-associated gene-A (CagA) positive strains, stimulate the release of a variety of proinflammatory cytokines, including interleukin-1 (IL-1), interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α ) (Perri et al 1999;Russo et al 2001). The eradication of H. pylori leads to normalization of serum cytokines levels (Kountouras et al 2000).…”

Pro- and Antiphlogistic Concentration of Cytokines in Rats’ Serum after Long-Term Administration of Omeprazole and the Simultaneous Injection of Multiprobiotics and Omeprazole

“…З 90-х років минулого століття почина-ються інтенсивні дослідження етіологічної ролі H. pylori не тільки в розвитку виразкової хвороби, але і в запаленні слизової оболонки шлунку. Зага-льноприйнято, що в основі виразкової і пухлинної хвороби шлунка, а також запальних захворювань кишечника лежить хронічне запалення, викликане H. pylori [8,12,14,21,27,30]. Що стосується ролі цитокінів у запальному процесі в шлунку і кишечни-ку, що розвивається на фоні тривалої гіпоациднос-ті шлункового соку за відсутності H. pylori інфіку-вання, дані літератури обмежені і стосуються лише окремих цитокінів.…”

The C-Terminal Disulfide Bonds of Helicobacter pylori GroES Are Critical for IL-8 Secretion via the TLR4-Dependent Pathway in Gastric Epithelial Cells

“…It is well recognized that release of these proinflammatory cytokines is closely linked to the pathogenesis of H. pylori-associated gastric cancer (12,13). Induction of cytokine secretion by H. pylori depends on both the host genetic background and microbial virulence (9). Among these cytokines, IL-8 is the most highly expressed gene in H. pylori-infected gastric epithelial cells and appears to play a major role in the epithelial cell response to H. pylori infection and in the pathological processes leading to gastric disease (14,15).…”

“…The most remarkable feature of persistent H. pylori infection is that it causes inflammatory responses, which is an important risk factor for malignancy (3). H. pylori infection induces gastritis with infiltration of neutrophils, macrophages, dendritic cells, as well as T and B lymphocytes into the gastric mucosa (4)(5)(6)(7)(8) in addition to the accumulation of various cytokines, including TNF-a, IL-1b, IL-6, and IL-8 secreted by gastric epithelial and immune cells (9)(10)(11). It is well recognized that release of these proinflammatory cytokines is closely linked to the pathogenesis of H. pylori-associated gastric cancer (12,13).…”