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Proinflammatory cytokine expression in gastric tissue from children with Helicobacter pylori-associated gastritis
E Guiraldes1, I Duarte, A Peña
1Departamentos de Pediatría y Anatomía Patológica, Pontificia Universidad Católica de Chile, Santiago, Chile. eguirald@puc.cl
Insights
Helicobacter pylori infection in children increases gastric mucosal production of interleukin-1 beta (IL-1β) and interleukin-8 (IL-8). These inflammatory cytokines are linked to H. pylori-associated gastric damage and varied clinical outcomes in pediatric patients.
Area of Science:
- Pediatric Gastroenterology
- Infectious Diseases
- Immunology
Background:
- Helicobacter pylori (H. pylori) infection is common in childhood, leading to chronic gastric inflammation.
- Inflammatory cytokines are elevated during chronic inflammation, but data in children are limited.
- Understanding cytokine involvement in pediatric H. pylori infection is crucial for managing gastric damage.
Purpose of the Study:
- To investigate the concentrations of key inflammatory cytokines in the gastric mucosa of H. pylori-infected children.
- To correlate cytokine levels with clinical, histologic, and sociodemographic factors.
- To elucidate the role of specific cytokines in H. pylori-associated gastric pathology in pediatric populations.
Main Methods:
- Studied 79 children (ages 5-18) undergoing upper gastrointestinal endoscopy in Chile.
- Measured concentrations of IL-1β, IL-6, IL-8, and TNF-α in gastric mucosal biopsies.
- Utilized reverse transcription polymerase chain reaction (RT-PCR) for cytokine expression analysis and correlated data with patient status.
Main Results:
- H. pylori colonization was inversely related to socioeconomic status and positively to age.
- Significantly higher IL-1β, IL-8, and TNF-α levels were found in H. pylori-positive children and those with gastritis.
- Elevated IL-1β and IL-8 were observed in children with peptic ulcer disease; IL-6 levels were comparable across groups.
Conclusions:
- Increased gastric mucosal production of IL-1β and IL-8 is likely involved in H. pylori-induced gastric damage in children.
- These cytokines may play a critical role in determining diverse clinical outcomes of H. pylori infection in pediatric patients.
- The findings highlight the importance of specific inflammatory mediators in pediatric H. pylori pathogenesis.
Background:
Helicobacter pyloriinfection of the gastric mucosa in humans is usually acquired early in life. The chronic inflammation that ensues involves the increased production of inflammatory cytokines. Published data on production of these mediators by gastric mucosa of H. pylori-infected children are few.
Methods:
Seventy-nine children, aged 5 to 18 years, referred for upper gastrointestinal endoscopy to four separate hospitals in Chile, were studied. The concentrations of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor alpha were measured in homogenates of gastric mucosal biopsy specimens. Cytokine expression was confirmed by reverse transcription polymerase chain reaction. These data were correlated with the patients' clinical, histologic and sociodemographic status.
Results:
Patient rate of colonization by H. pylori was inversely correlated with socioeconomic status (P < 0.005) and positively correlated with age (P < 0.0025). In gastric mucosa, concentrations of IL-1beta, IL-8, and tumor necrosis factor alpha were all significantly higher in H. pylori-positive patients than in H. pylori-negative patients and in patients who had histologic gastritis than in those with normal gastric mucosa. In patients with peptic ulcer disease, only IL-1beta and IL-8 concentrations were significantly elevated when compared with those of patients without ulcers. Interleukin-6 concentrations were comparable among the different groups analyzed.
Conclusions:
This study suggests that increased gastric mucosal production of the proinflammatory cytokines IL-1beta and IL-8 is probably involved in H. pylori-associated gastric damage in children and may be crucial in determining the different clinical outcomes.