Density of Helicobacter pylori infection in vivo as assessed by quantitative culture and histology

被引:173
作者
Atherton, JC
Tham, KT
Peek, RM
Cover, TL
Blaser, MJ
机构
[1] VANDERBILT UNIV,SCH MED,DEPT MED A3310 MCN,DIV INFECT DIS,NASHVILLE,TN 37232
[2] VANDERBILT UNIV,SCH MED,DEPT MED,DIV GASTROENTEROL,NASHVILLE,TN 37212
[3] VANDERBILT UNIV,SCH MED,DEPT PATHOL,NASHVILLE,TN 37212
[4] DEPT VET AFFAIRS MED CTR,DEPT PATHOL,NASHVILLE,TN 37212
[5] DEPT VET AFFAIRS MED CTR,MED SERV,NASHVILLE,TN 37212
关键词
D O I
10.1093/infdis/174.3.552
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Helicobacter pylori density was assessed by quantitative culture and histologic examination of gastric biopsy specimens from 29 H. pylori-infected dyspeptic patients. Density was correlated with cagA and vacA genotypes (assessed by polymerase chain reaction and colony hybridization), gastric inflammation and epithelial injury (assessed histologically), and peptic ulceration. Quantitative culture was more reproducible than histology, and antral density was more reproducible than corpus density. Mean antral density of cagA(+)/vacA s1 strains was 4-fold higher than that of cagA(-)/vacA s2 strains (1.9 x 10(6) vs. 4.5 x 10(5) cfu/g, P =.02). Antral density was associated with mucosal neutrophilic and lymphocytic infiltration (P <.01) and with epithelial injury (P <.05). Mean antral bacterial density was 5-fold higher in duodenal ulcer patients than in others (P =.005). In conclusion, H. pylori density in vivo is easily quantified and is associated with bacterial virulence determinants, gastric inflammation, and duodenal ulceration, suggesting a central role in pathogenesis.
引用
收藏
页码:552 / 556
页数:5
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