Effects of Helicobacter pylori on biological characteristics of gastric epithelial cells
Ping Wang1,2,3, Juan Mei3, Jing Tao4, Ning Zhang2, Hua Tian2 and Guo-Hui Fu2
1Department of Pathology, Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China, 2Department of Pathology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Institutes of Medical Sciences, Shanghai JiaoTong University School of Medicine, Shanghai, P.R. China, 3Department of Pathology, Bengbu Medical College, Bengbu, China and 4Department of Medical Microbiology and Parasitology, Institutes of Medical Sciences, Shanghai JiaoTong University School of Medicine, Shanghai, China.
Offprint requests to: Guo-Hui Fu, M.D., Ph.D., Department of Pathology, Shanghai Jiao Tong University, School of Medicine, No.280, South Chong-Qing Road, Shanghai, 200025, P.R. China. e-mail: fuguhu@263.net
Summary. Infection with Helicobacter pylori (H. pylori) strains is linked to an increased risk of inflammation and gastric cancer. To investigate the effects of H. pylori on biological characteristics of gastric epithelial cells SGC-7901, derived from human adenocarcinoma, morphological appearances of both the pathogen and these cells, as well as features of attachment and internalization were observed by using transmission electron microscopy (TEM). We also investigated cell junctions and invasion by TEM and Transwell Invasion Assay. Cell proliferation and apoptosis were assessed by using chromogenic methylthiazol tetrazolium bromide (MTT) dye and flow cytometry. Three types of H. pylori were observed around, attaching to, or invading tumor cells. Cellular damage was characterized by vacuolar degeneration, dilated endoplasmic reticulum (ER), and reduction of organelles. Cell junctions and cell microvilli reduced or disappeared. H. pylori inhibited cell proliferation, whereas it had no effect on apoptosis. It also promoted gastric carcinoma cell invasion. H. pylori damages cell construction, destroys cell junctions, inhibits cell proliferation, promotes cell invasive ability, and, therefore, might accelerate the malignant progress and metastasis of gastric cancer. Histol Histopathol 27, 1079-1091 (2012)
Key words: Helicobacter pylori, Gastric carcinoma, Invasion, Ultrastructure, Apoptosis, Proliferation
DOI: 10.14670/HH-27.1079