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Epidemiologic studies have reported an inverse relationship between childhood  Helicobacter pylori  infection and development of allergic asthma. Because lung epithelium plays an important role in allergic asthma pathogenesis, we hypothesized that  H .  pylori  may directly influence airway epithelial cell innate immune function, particularly in early childhood. To test our hypothesis, we established an  in vitro H .  pylori  infection model using primary tracheobronchial epithelial cell cultures derived from infant, juvenile and adult rhesus monkeys. Airway epithelial cell cultures were infected with wild-type or cag pathogenicity island mutant  H .  pylori  strains, followed by evaluation of IL-8 and IL-6 protein synthesis. We found that  H .  pylori  primarily increased IL-8 synthesis in a MOI and age-dependent fashion, with a greater than 4-fold induction in infant versus adult cultures.  H .  pylori -induced IL-8 synthesis in infant and juvenile cultures was significantly reduced by cag pathogenicity island mutants, indicating a requirement for the type IV secretion system. Although peptidoglycan recognition of nucleotide binding oligomerization domain-containing protein 1 (NOD1) and NF-kappaB have been implicated as key cytokine signaling molecules for  H .  pylori  infection in gastric epithelium, NOD1 (ML130) or NF-kappaB (JSH-23) inhibitors minimally affected IL-8 synthesis in airway epithelial cell cultures following  H .  pylori  infection. In contrast, inhibition of the p38 MAP kinase pathway (SB203580) resulted in almost complete suppression of  H .  pylori -induced IL-8 synthesis. Collectively, these results indicate that  H .  pylori  can preferentially elicit IL-8 synthesis in a model of pediatric airway epithelium using the type IV secretion system via p38 MAP kinase.

The Helicobacter pylori type IV secretion system promotes IL-8 synthesis in a model of pediatric airway epithelium via p38 MAP kinase