Host adaptation and immune modulation are mediated by homologous recombination in Helicobacter pylori

被引：32

作者：

Robinson, K

Loughlin, MF

Potter, R

Jenks, PJ

机构：

[1] Univ Nottingham, Queens Med Ctr, Inst Infect Immun & Inflammat, Nottingham NG7 2UH, England

[2] Univ Nottingham, Queens Med Ctr, Wolfson Digest Dis Ctr, Nottingham NG7 2UH, England

来源：

JOURNAL OF INFECTIOUS DISEASES | 2005年 / 191卷 / 04期

基金：

英国惠康基金;

关键词：

D O I：

10.1086/427657

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Rearrangement of genomic DNA via homologous recombination provides an alternative mechanism of gene regulation that is essential for successful colonization of the gastric mucosa by Helicobacter pylori. Inoculation of outbred mice with the H. pylori SS1 wild-type strain elicited a T helper (Th) 2 response and established a persistent infection. In contrast, inoculation with an isogenic H. pylori strain defective for homologous recombination elicited a Th1-mediated immune response and clearance of infection within 70 days. We, therefore, demonstrate that recombination is critical for mediating persistence of a microbial pathogen through the induction of ineffective immune responses.

引用

收藏

页码：579 / 587

页数：9

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