Dangerous Liaison: Helicobacter pylori, Ganglionitis, andMyenteric Gastric Neurons: A Histopathological Study

Chronic inflammation induced byHelicobacter pylori(H. pylori) infection plays a major role in development of gastric cancer.However, recentfindings suggested that progression of inflammation and neoplastic transformation inH. pyloriinfection aremore complex than previously believed and could involve different factors that modulate gastric microenvironment andinfluence host-pathogen interaction. Among these factors, gastric myenteric plexus and its potential adaptive changes in H.pylori infection received little attention. This study is aimed at identifying the impact ofH. pylori-associated gastritis on numberand morphology of nerve cells in the stomach. The distribution of density, inflammation, and programmed cell death inneurons was immunohistochemically assessed in full-thickness archival tissue samples obtained from 40 patients withH. pyloriinfection who underwent surgery for gastric cancer and were compared withfindings on samples collected from 40 age- andsex-matched subjects without bacteria. Overall, significant differences were noted betweenH. pylori-positive andH. pylori-negative patients. The analysis of tissue specimens obtained from those with infection revealed higher density and larger surfaceof the myenteric nervous plexus, as well as a significant increase in the number of gastric neuronal cell bodies and glial cellscompared to controls. A predominant CD3-immunoreactive T cell infiltrate confined to the myenteric plexus was observed ininfected subjects. The presence of mature B lymphocytes, plasma cells, and eosinophils was also noted, but to a lesser extent,within the ganglia. Myenteric ganglionitis was associated with degeneration and neuronal loss. Our results represent thefirsthistopathological evidence supporting the hypothesis thatH. pylori-induced gastric inflammation may induce morphologicalchanges in myenteric gastric ganglia. Thesefindings could help gain understanding of some still unclear aspects of pathogenesisofH. pyloriinfection, with the possibility of having broader implications for gastric cancer progression.