Helicobacter heilmannii sensu lato‐induced MALT Lymphoma Formation in Lacrimal Gland as well as Fundic Gland in C57BL/6 mouse: Effect of Aprepitant

Abstract

As to the pathogenesis of the Sjogren syndrome, Helicobacter pylori has been suggested to have some relation mostly from the epidemiological studies, while few experimental studies have clarified this point.We have established a gastric low‐grade MALT lymphoma model in C57BL/6 mouse by the infection of Helicobacter heilmannii sensu lato obtained from cynomolgus monkey. After the long term infection, we have detected the accumulation of lymphocytes in the lacrimal glands similar to the gastric MALT lymphoma. The characteristics of this lesion were investigated as well as the effect of aprepitant, an NK‐1R antagonist on this lesion.Materials and MethodsThe characteristics of the lymphocyte accumulation were investigated by the histochemical analysis using lymphocyte marker, CD4, B220, CD10, epithelial cell marker cytokeratin, mucus marker MUC7 and aquaporin‐4 and 5. The localization of the autonomic nerves was also clarified by the choline acetyltransferase, substance P and calcitonin gene‐related peptide.ResultsBy the histochemical analysis, the lymphoepithelial lesion was detected in the lymphocyte aggregation and the germinal center was formed in the center of the lesion, showing its characteristics as a mucosa‐associated lymphoid tissue (MALT) lymphoma. The lesion was also richly innervated by the autonomic nerves. Intraperitoneal administration of aprepitant induced the significant reduction in the lesion size.ConclusionHelicobacter heilmannii sensu lato infection to the C57BL/6 mouse induced the formation of the MALT lymphoma in the mouse lacrimal gland. This model could be one of the animal models of the Sjogren syndrome.