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Approximately 50% of the world's population is infected withHelicobacter pylori , leading to chronic inflammation, which increases the risk for gastric adenocarcinoma. MyD88 is a key adaptor molecule in inflammatory pathways involved in interleukin 1 (IL-1)/IL-18/Toll-like receptor signaling and has been shown to have divergent effects in carcinogenesis. The role of MyD88 inHelicobacter -induced gastric malignancy is unknown. Using a mouse model ofHelicobacter -induced gastric cancer, we assessed the role of MyD88 in cancer development by evaluating gastric histopathology, apoptosis, proliferation, and cytokine expression. Infection of MyD88-deficient (Myd88 −/− ) mice withHelicobacter resulted in early and rapid advancement to gastric dysplasia as early as 25 weeks postinfection. The progression ofHelicobacter -induced disease to precancerous and cancerous lesions in the absence of MyD88 signaling was accompanied by increased gastric epithelial apoptosis and proliferation. In addition, inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), gamma interferon (IFN-γ), IL-6, and IL-1β were highly expressed in association with the development of gastric dysplasia. These data suggest that MyD88 signaling retards development and progression to cancer duringHelicobacter infection. This is the first study to show evidence of MyD88 protection in an infection-driven inflammation-associated cancer model.

infection and immunity

Deficiency of the Myeloid Differentiation Primary Response Molecule MyD88 Leads to an Early and Rapid Development of Helicobacter-Induced Gastric Malignancy