Enhanced Susceptibility to Citrobacter rodentium Infection in MicroRNA-155-Deficient Mice

被引：31

作者：

Clare, Simon ^{[1
]}

John, Victoria ^{[1
]}

Walker, Alan W. ^{[1
]}

Hill, Jennifer L. ^{[1
]}

Abreu-Goodger, Cei ^{[2
]}

Hale, Christine ^{[1
]}

Goulding, David ^{[1
]}

Lawley, Trevor D. ^{[1
]}

Mastroeni, Pietro ^{[5
]}

Frankel, Gadi ^{[4
]}

Enright, Anton J. ^{[2
]}

Vigorito, Elena ^{[3
]}

Dougan, Gordon ^{[1
]}

机构：

[1] Wellcome Trust Sanger Inst, Cambridge, England

[2] EMBL European Bioinformat Inst, Cambridge, England

[3] Babraham Inst, Cambridge, England

[4] Univ London Imperial Coll Sci Technol & Med, London, England

[5] Univ Cambridge, Dept Vet Med, Cambridge, England

来源：

INFECTION AND IMMUNITY | 2013年 / 81卷 / 03期

基金：

英国惠康基金;

关键词：

INFLAMMATORY-BOWEL-DISEASE; MURINE COLONIC HYPERPLASIA; CD4(+) T-CELLS; IN-VIVO; GERMINAL-CENTERS; PATHOGEN; IMMUNITY; COLITIS; GENE; COLONIZATION;

D O I：

10.1128/IAI.00969-12

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

MicroRNAs (miRNAs) are small noncoding molecules that control gene expression posttranscriptionally, with microRNA-155 (miR-155) one of the first to be implicated in immune regulation. Here, we show that miR-155-deficient mice are less able to eradicate a mucosal Citrobacter rodentium infection than wild-type C57BL/6 mice. miR-155-deficient mice exhibited prolonged colonization associated with a higher C. rodentium burden in gastrointestinal tissue and spread into systemic tissues. Germinal center formation and humoral immune responses against C. rodentium were severely impaired in infected miR-155-deficient mice. A similarly susceptible phenotype was observed in mu MT mice reconstituted with miR-155-deficient B cells, indicating that miR-155 is required intrinsically for mediating protection against this predominantly luminal bacterial pathogen.

引用

页码：723 / 732

页数：10