INDUCTION OF VARIOUS CYTOKINES AND DEVELOPMENT OF SEVERE MUCOSAL INFLAMMATION BY CAGA GENE POSITIVE HELICOBACTER-PYLORI STRAINS

Citation
Y. Yamaoka et al., INDUCTION OF VARIOUS CYTOKINES AND DEVELOPMENT OF SEVERE MUCOSAL INFLAMMATION BY CAGA GENE POSITIVE HELICOBACTER-PYLORI STRAINS, Gut, 41(4), 1997, pp. 442-451
Citations number
29
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
GutACNP
ISSN journal
00175749
Volume
41
Issue
4
Year of publication
1997
Pages
442 - 451
Database
ISI
SICI code
0017-5749(1997)41:4<442:IOVCAD>2.0.ZU;2-Y
Abstract
Background-Helicobacter pylori strains possessing the cagA gene are th ought to induce interleukin 8 (IL-8) in gastric mucosa. However, it is still unclear whether a relation exists between the cagA gene and the expression patterns of cytokines other than IL-8. Aims-To investigate the relation between the cagA gene and the production of various cyto kine proteins using an enzyme linked immunosorbent assay (ELISA). Pati ents and methods-In 184 patients, the cagA gene was detected by polyme rase chain reaction (PCR), and levels of production of IL-1 beta, IL-6 , IL-7, IL-8, IL-10, and tumour necrosis factor alpha (TNF-alpha) in a ntral biopsy specimens were measured by ELISA. Results-Mucosal levels of IL-1 beta, IL-6, IL-8, and TNF-alpha were significantly higher in H pylori positive than in H pylori negative patients. Furthermore, the mucosal levels of IL-1 beta and IL-8 were significantly higher in spec imens infected with cagA positive strains than in those infected with cagA negative strains. In H pylori positive patients, the mucosal leve l of IL-8 was closely correlated with that of IL-1 beta (p<0.0001), an d the mucosal level of IL-6 was closely correlated with that of TNF-al pha (p<0.0001). Conclusion-These findings suggest that the ability to induce cytokines differs among the strains; cagA(+) strains induce var ious kinds of cytokines and may cause severe inflammation, whereas cag A(-) strains induce IL-8 and IL-1 beta only weakly and may cause only mild inflammation. However, as most patients infected with the cagA(+) strains have gastritis, these strains may not be equivalent to ulcero genic strains.