In:
Journal of Clinical Microbiology, American Society for Microbiology, Vol. 38, No. 6 ( 2000-06), p. 2215-2218
Abstract:
The aim of this study was to investigate the effect of Helicobacter pylori on the function of gastric mucous cells. H. pylori (10 4 to 10 7 CFU/well) was incubated with the mucin-producing gastric cell line HM02 for 12 and 24 h. Mucin synthesis and secretion were determined by the incorporation of d - N -[ acetyl - 14 C]glucosamine into intracellular and released high-molecular-weight glycoproteins. cagA -positive, cytotoxin-producing and non-cytotoxin-producing H. pylori strains impaired the incorporation of d - N -[ acetyl - 14 C]glucosamine into intracellular glycoproteins. Significant inhibition of mucin synthesis was noted after 12 and 24 h of cocultivation with a bacterial load of ≥10 5 bacteria (bacterium/cell ratio = 0.25). The cagA -positive, cytotoxin-producing strains (HP64, HP57, and HP87) caused significantly stronger inhibition of intracellular mucin synthesis than the cagA -positive, non-cytotoxin-producing strains (HP05, HP83, and HP84). The cagA -negative, non-cytotoxin-producing strains (HP01, HP04, and HP85) did not affect intracellular mucin synthesis. The results indicate that H. pylori directly impairs mucin synthesis in gastric mucous cells and that cytotoxic cagA -positive strains cause more profound inhibition of mucin synthesis. We suggest that the increased inhibitory effect of cagA -positive, cytotoxin-producing strains on mucin synthesis can be considered one possible factor responsible for the increased risk of developing peptic ulceration with these H. pylori strains.
Type of Medium:
Online Resource
ISSN:
0095-1137
,
1098-660X
DOI:
10.1128/JCM.38.6.2215-2218.2000
Language:
English
Publisher:
American Society for Microbiology
Publication Date:
2000
detail.hit.zdb_id:
1498353-9
SSG:
12
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