Effects of Helicobacter pylori infection on cell cycle progression and the expression of cell cycle regulatory proteins

被引:10
作者
De Luca, A
De Falco, M
Iaquinto, S
Iaquinto, G
机构
[1] Univ Naples 2, Dept Med & Publ Hlth, Sect Clin Anat, I-80138 Naples, Italy
[2] Univ Naples Federico II, Dept Evolut & Comparat Biol, Naples, Italy
关键词
D O I
10.1002/jcp.20022
中图分类号
Q2 [细胞生物学];
学科分类号
071009 [细胞生物学]; 090102 [作物遗传育种];
摘要
Helicobacter pylori lives in the stomach lumen adhering and specifically inter acting with gastric epithelial cells. H. pylori infection can cause a broad range of diseases. Although most infected individuals only develop a chronic inflammation of the stomach; some patients progress to chronic gastritis, duodenal ulceration, or, rarely, cancer. H: pylori. is able to send and to receive signals from the gastric epithelium, allowing host and bacteria to become linked in a dynamic equilibrium. Several studies have demonstrated that H. pylori infection induces morphological changes of gastric epithelial cells other than cell proliferation, increase of mitosis and mutations. It has also been demonstrated that H. pylori may predispose to cancer by altering gastric epithelial cell turnover actin specifically on transcription factors. Although H. pylori is able to induce several host responses, it specifically perturbs the delicate balance of those factors that usually help to maintain Cell. homeostasis. The study of mechanisms of interaction between the bacterium and gastric cells will surely help to prevent the increase and diffusion of malignancies all over the world. (C) 2004 Wiley-Liss, Inc.
引用
收藏
页码:334 / 342
页数:9
相关论文
共 120 条
[1]
Mechanisms involved in Helicobacter pylori-induced interleukin-8 production by a gastric cancer cell line, MKN45 [J].
Aihara, M ;
Tsuchimoto, D ;
Takizawa, H ;
Azuma, A ;
Wakebe, H ;
Ohmoto, Y ;
Imagawa, K ;
Kikuchi, M ;
Mukaida, N ;
Matsushima, K .
INFECTION AND IMMUNITY, 1997, 65 (08) :3218-3224
[2]
Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori [J].
Alm, RA ;
Ling, LSL ;
Moir, DT ;
King, BL ;
Brown, ED ;
Doig, PC ;
Smith, DR ;
Noonan, B ;
Guild, BC ;
deJonge, BL ;
Carmel, G ;
Tummino, PJ ;
Caruso, A ;
Uria-Nickelsen, M ;
Mills, DM ;
Ives, C ;
Gibson, R ;
Merberg, D ;
Mills, SD ;
Jiang, Q ;
Taylor, DE ;
Vovis, GF ;
Trost, TJ .
NATURE, 1999, 397 (6715) :176-180
[3]
TOO MANY RODENT CARCINOGENS - MITOGENESIS INCREASES MUTAGENESIS [J].
AMES, BN ;
GOLD, LS .
SCIENCE, 1990, 249 (4972) :970-971
[4]
THE ROLE OF JUN, FOS AND THE AP-1 COMPLEX IN CELL-PROLIFERATION AND TRANSFORMATION [J].
ANGEL, P ;
KARIN, M .
BIOCHIMICA ET BIOPHYSICA ACTA, 1991, 1072 (2-3) :129-157
[5]
[Anonymous], BIOCH BIOPHYS ACTA
[6]
Importance of changes in epithelial cell turnover during Helicobacter pylori infection in gastric carcinogenesis [J].
Anti, M ;
Armuzzi, A ;
Gasbarrini, A ;
Gasbarrini, G .
GUT, 1998, 43 :S27-S32
[7]
Helicobacter pylori CagA protein can be tyrosine phosphorylated in gastric epithelial cells [J].
Asahi, M ;
Azuma, T ;
Ito, S ;
Ito, Y ;
Suto, H ;
Nagai, Y ;
Tsubokawa, M ;
Tohyama, Y ;
Maeda, S ;
Omata, M ;
Suzuki, T ;
Sasakawa, C .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 191 (04) :593-602
[8]
MOSAICISM IN VACUOLATING CYTOTOXIN ALLELES OF HELICOBACTER-PYLORI - ASSOCIATION OF SPECIFIC VACA TYPES WITH CYTOTOXIN PRODUCTION AND PEPTIC-ULCERATION [J].
ATHERTON, JC ;
CAO, P ;
PEEK, RM ;
TUMMURU, MKR ;
BLASER, MJ ;
COVER, TL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (30) :17771-17777
[9]
Translocation of the Helicobacter pylori CagA protein in gastric epithelial cells by a type IV secretion apparatus [J].
Backert, S ;
Ziska, E ;
Brinkmann, V ;
Zimny-Arndt, U ;
Fauconnier, A ;
Jungblut, PR ;
Naumann, M ;
Meyer, TF .
CELLULAR MICROBIOLOGY, 2000, 2 (02) :155-164
[10]
Baik SC, 1996, CANCER RES, V56, P1279