Pathogenesis of Helicobacter pylori infection

被引:21
作者
Lamarque, D
Peek, RM [1 ]
机构
[1] Vanderbilt Univ, Div Gastroenterol, Sch Med,Dept Med, Med Ctr N C 2104, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Div Gastroenterol, Sch Med, Dept Canc Biol, Nashville, TN 37232 USA
[3] Hop Bichat Claude Bernard, Serv Hepatogastroenterol, F-75877 Paris, France
[4] Dept Vet Affairs Med Ctr, Nashville, TN 37212 USA
关键词
adherence; apoptosis; inflammation; pathogenesis; persistence; virulence;
D O I
10.1046/j.1523-5378.2003.00166.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Helicobacter pylori induces persistent inflammation in the human stomach, yet only a minority of colonized persons develop peptic ulcer disease or gastric malignancy. Numerous studies published in the last year have demonstrated that H. pylori isolates possess substantial phenotypic and genotypic diversity, which may engender differential host inflammatory responses that influence clinical outcome. Results from these recent investigations have more precisely delineated the mechanisms of H. pylori pathogenesis, which will ultimately help to define colonized persons bearing the highest risk for disease, and enable physicians to appropriately focus diagnostic testing and eradication therapy.
引用
收藏
页码:21 / 30
页数:10
相关论文
共 58 条
[1]   Helicobacter pylori enter and survive within multivesicular vacuoles of epithelial cells [J].
Amieva, MR ;
Salama, NR ;
Tompkins, LS ;
Falkow, S .
CELLULAR MICROBIOLOGY, 2002, 4 (10) :677-690
[2]   Two predicted chemoreceptors of Helicobacter pylori promote stomach infection [J].
Andermann, TM ;
Chen, YT ;
Ottemann, KM .
INFECTION AND IMMUNITY, 2002, 70 (10) :5877-5881
[3]  
Ando T, 2002, CANCER RES, V62, P2385
[4]   Cutting edge: Carbohydrate profiling identifies new pathogens that interact with dendritic cell-specific ICAM-3-grabbing nonintegrin on dendritic cells [J].
Appelmelk, BJ ;
van Die, I ;
van Vliet, SJ ;
Vandenbroucke-Grauls, CMJE ;
Geijtenbeek, TBH ;
van Kooyk, Y .
JOURNAL OF IMMUNOLOGY, 2003, 170 (04) :1635-1639
[5]  
Bäckhed F, 2003, J INFECT DIS, V187, P829
[6]   Modulation of host antimicrobial peptide (β-defensins 1 and 2) expression during gastritis [J].
Bajaj-Elliott, M ;
Fedeli, P ;
Smith, GV ;
Domizio, P ;
Maher, L ;
Ali, RS ;
Quinn, AG ;
Farthing, MJG .
GUT, 2002, 51 (03) :356-361
[7]   Immune-mediated neural dysfunction in a murine model of chronic Helicobacter pylori infection [J].
Bercík, P ;
De Giorgio, R ;
Blennerhassett, P ;
Verdú, EF ;
Barbara, G ;
Collins, SM .
GASTROENTEROLOGY, 2002, 123 (04) :1205-1215
[8]   Severe inflammation and reduced bacteria load in murine Helicobacter infection caused by lack of phagocyte oxidase activity [J].
Blanchard, TG ;
Yu, FW ;
Hsieh, CL ;
Redline, RW .
JOURNAL OF INFECTIOUS DISEASES, 2003, 187 (10) :1609-1615
[9]   Two different families of hopQ Alleles in Helicobacter pylori [J].
Cao, P ;
Cover, TL .
JOURNAL OF CLINICAL MICROBIOLOGY, 2002, 40 (12) :4504-4511
[10]   Effect of inhibition of extracellular signal-regulated kinase 1 and 2 pathway on apoptosis and bcl-2 expression in Helicobacter pylori-infected AGS cells [J].
Choi, IJ ;
Kim, JS ;
Kim, JM ;
Jung, HC ;
Song, IS .
INFECTION AND IMMUNITY, 2003, 71 (02) :830-837