Open AccessIncreased apoptosis and angiogenesis in gastric low‐grade mucosa‐associated lymphoid tissue‐type lymphoma by Helicobacter heilmannii infection in C57/BL6 mice
Author(s) -
Nishikawa Kaori,
Nakamura Masahiko,
Takahashi Shinichi,
Matsui Hidenori,
Murayama Somay Yamagata,
Matsumoto Tsukasa,
Yamada Haruki,
Tsuchimoto Kanji
Publication year - 2007
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2007.00252.x
Subject(s) - malt lymphoma , lymphoma , biology , lymphatic system , angiogenesis , pathology , bcl10 , mucosa associated lymphoid tissue , gastric mucosa , gastric lymphoma , vascular endothelial growth factor , apoptosis , stomach , immunology , cancer research , medicine , biochemistry , vegf receptors
Helicobacter heilmannii has been reported to cause gastric low‐grade mucosa‐associated lymphoid tissue‐type (MALT) lymphoma, but its precise pathophysiological mechanism remains to be clarified. We recently established a model of gastric B‐cell MALT lymphoma in C57BL/6 mice by means of peroral infection of H. heilmannii primarily obtained from cynomolgus monkeys. Using this model, macroscopic, immunohistochemical, and electron microscopic observations of MALT lymphomas were carried out in order to examine the development of apoptosis and angiogenesis. Enhancement of the microvascular network and an increase in vascular endothelial growth factor‐A were detected in the central region of the MALT lymphoma tissue in the infected mouse stomach, while vascular endothelial growth factor‐C was detected at the margins of the MALT lymphomas. In addition, many H. heilmannii ‐invaded parietal cells showed caspase‐3 immunoreactivity in the fundic mucosal tissue surrounding the MALT lymphoma. In conclusion, in H. heilmannii ‐induced MALT lymphoma, enhanced immunoreactivity of vascular endothelial growth factor‐A and factor‐C was observed in areas encircled by increased parietal cell apoptosis, which indicates the pathophysiological relevance of both angiogenesis and apoptosis in MALT lymphoma formation.