Cytokine Expression in PediatricHelicobacter pyloriInfection

Abstract

Helicobacter pylori infection is one of the most common gastrointestinal infections worldwide and almost invariably causes chronic gastritis in the infected host. A predominant Th1 profile has been demonstrated in H. pylori-infected mucosa from adults, but no previous study has evaluated in situ cytokine expression in children. We therefore examined expression of proinflammatory, anti-inflammatory, and regulatory cytokines by immunohistochemistry in cryopreserved antral biopsy specimens from 10 H. pylori-infected and 10 uninfected children and correlated expression of cytokines with histology scores. Concomitant expression of interleukin-8 (IL-8), gamma interferon (IFN-␥), IL-4, transforming growth factor ␤, and tumor necrosis factor alpha was seen in 8/10 H. pylori-infected cases and in 5/10 noninfected cases; all H. pylori-infected subjects showed staining for at least two of the cytokines. The proportion of epithelial cytokine-specific staining did not differ significantly between the groups, either in surface or glandular epithelium. Furthermore, no significant differences were noticed between intraepithelial or lamina propria lymphocyte staining in the groups. There was, however, a tendency of higher numbers of IFN-␥-and IL-8-positive cells in the H. pylori-infected group. IFN-␥ and IL-8 lamina propria lymphocyte expression correlated significantly with antrum chronic inflammation, but there was no correlation between histology scores and epithelial cytokine expression. When the same techniques were used, the cytokine response appeared to be smaller in H. pylori-infected children than in adults, and there was no clear Th1 dominance. These results therefore suggest a different mucosal immunopathology in children. It remains to be determined whether the gastric immune response is downregulated in children with H. pylori infection and whether this is relevant to the outcome of infection.

Lactobacilli inhibit interleukin-8 production induced by Helicobacter pylori lipopolysaccharide-activated Toll-like receptor 4

“…Some studies [1][2][3][4][5] demonstrated that H pylori can stimulate interleukin-8 (IL-8) production in gastric mucosal epithelia, which induces accumulation of neutrophilic granulocytes in mucosa. Chemotactic response initiates inflammatory damage to gastric mucosa, which plays a crucial role in the pathogenesis of H pylori.…”

Lymphocyte Apoptosis, Proliferation and Cytokine Synthesis Pattern in Children with Helicobacter pylori Infection

“…Low IL-12 production may play a role in a complex and still poorly understood mechanism of rather limited H. pylori-mediated pro-inflammatory responses usually observed in children (Bontems at al. 2003, Lopes et al 2005). …”

Helicobacter pylori—Associated Dyspepsia in Paediatrics

“…Indeed, adults exhibit a predominantly neutrophil infiltrate, whereas H. pylori-associated gastritis in children is usually mild and superficial with a predominantly mononuclear infiltrate, a paucity of neutrophils and a higher degree of lymphoid follicular hyperplasia [118]. Therefore, different immunopathology and different patterns of cytokine expression would be anticipated for children when compared to adults [18]. There may be differences in adaptive component of gastric mucosa immune response in children compared to the adult host; a clear Th1 response has not always been demonstrated for young patients.…”

“…Nevertheless, H. pylori-associated peptic ulcer disease may also occur shortly after infection in childhood [4][5][6][7][8]. This rare event may be due to more virulent strains [9][10][11][12][13][14][15][16], and/or more predisposed subjects [17][18][19]. The two forms of H. pylori-associated peptic ulcers, i.e., gastric ulcer and duodenal ulcers, are divergent in prevalence and physiopathology, but both cause considerable patients' morbidity entailing high annual costs of treatment [93].…”

“…If often asymptomatic, the H. pylori-associated non-ulcer dyspepsia is clearly the strongest aetiological factor for severe gastric diseases that will develop late in adult life in a minority of infected patients, i.e., peptic ulcer disease, both gastric and duodenal ulcers, and gastric cancer, namely, adenocarcinoma and mucosa associated lymphoid tissue (MALT) lymphoma (reviewed in [3]). Peptic ulcer disease rarely occurs soon after H. pylori infection [4][5][6][7][8] that generally starts in childhood; this presumably reflects marked differences in the virulence [9][10][11][12][13][14][15][16] and/or in the susceptibility of young patients [17][18][19].…”