Specific strains of Escherichia coli are pathogenic for the endometrium of cattle and cause pelvic inflammatory disease in cattle and mice.
Specific strains of Escherichia coli are pathogenic for the endometrium of cattle and cause pelvic inflammatory disease in cattle and mice.
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DOI：
10.1371/journal.pone.0009192
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发表时间：
2010-02-12
期刊：
影响因子：
3.7
通讯作者：
Simpson KW
中科院分区：
文献类型：
--
作者：
Sheldon IM;Rycroft AN;Dogan B;Craven M;Bromfield JJ;Chandler A;Roberts MH;Price SB;Gilbert RO;Simpson KW
大肠杆菌广泛存在于环境中，致病菌株可引起包括女性生殖道在内的粘膜表面疾病。盆腔炎（PID;子宫炎）或盆腔炎影响分娩后约40%的牛。我们测试了多种遗传多样的E。分娩后环境中的大肠杆菌机会性地污染子宫腔以建立PID。E.应用随机扩增多态性DNA（RAPD）和多位点序列分型（MLST）技术，从子宫病动物标本中鉴定出10株大肠杆菌，与已知的肠内或肠外致病性大肠杆菌不同。杆菌子宫内膜致病性E. coli（EnPEC）对子宫内膜上皮细胞和间质细胞的粘附性和侵袭性均高于E.从临床上未受影响的动物的子宫中分离的大肠杆菌。与非致病性E.杆菌当EnPEC或其LPS输注到小鼠子宫中时，也引起PID，在子宫内膜中积聚中性粒细胞和巨噬细胞。EnPEC输注仅与子宫内膜和子宫肌层的细菌侵入相关。尽管EnPEC具有侵入培养细胞、引发宿主细胞反应和建立PID的能力，但它们缺乏16个通常与肠或肠外致病性E.大肠杆菌，虽然铁耶尔森菌素摄取基因（fyuA）存在于PID相关的EnPEC。来自野生型而非Toll样受体4（TLR 4）缺失小鼠的子宫内膜上皮或基质细胞分泌前列腺素E2和趋化因子（C-X-C基序）配体1（CXCL 1），以响应来自EnPEC的LPS，突出了LPS在PID中的关键作用。EnPEC的发现意味着PID的治疗或疫苗的开发应特别关注EnPEC，而不是其他E菌株。杆菌
Escherichia coli are widespread in the environment and pathogenic strains cause diseases of mucosal surfaces including the female genital tract. Pelvic inflammatory disease (PID; metritis) or endometritis affects ∼40% of cattle after parturition. We tested the expectation that multiple genetically diverse E. coli from the environment opportunistically contaminate the uterine lumen after parturition to establish PID. Distinct clonal groups of E. coli were identified by Random Amplification of Polymorphic DNA (RAPD) and Multilocus sequence typing (MLST) from animals with uterine disease and these differed from known diarrhoeic or extra-intestinal pathogenic E. coli. The endometrial pathogenic E. coli (EnPEC) were more adherent and invasive for endometrial epithelial and stromal cells, compared with E. coli isolated from the uterus of clinically unaffected animals. The endometrial epithelial and stromal cells produced more prostaglandin E2 and interleukin-8 in response to lipopolysaccharide (LPS) purified from EnPEC compared with non-pathogenic E. coli. The EnPEC or their LPS also caused PID when infused into the uterus of mice with accumulation of neutrophils and macrophages in the endometrium. Infusion of EnPEC was only associated with bacterial invasion of the endometrium and myometrium. Despite their ability to invade cultured cells, elicit host cell responses and establish PID, EnPEC lacked sixteen genes commonly associated with adhesion and invasion by enteric or extraintestinal pathogenic E. coli, though the ferric yersiniabactin uptake gene (fyuA) was present in PID-associated EnPEC. Endometrial epithelial or stromal cells from wild type but not Toll-like receptor 4 (TLR4) null mice secreted prostaglandin E2 and chemokine (C-X-C motif) ligand 1 (CXCL1) in response to LPS from EnPEC, highlighting the key role of LPS in PID. The implication arising from the discovery of EnPEC is that development of treatments or vaccines for PID should focus specifically on EnPEC and not other strains of E. coli.
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DOI：
10.1073/pnas.0607898104
发表时间：
2007-10-16
影响因子：
11.1
作者：
Lane, M. Chelsea;Alteri, Christopher J.;Mobley, Harry L. T.
通讯作者：
Mobley, Harry L. T.
影响因子：
56.9
作者：
Ernst, RK;Yi, EC;Miller, SI
通讯作者：
Miller, SI
影响因子：
10.7
作者：
Escobar-Páramo, P;Clermont, O;Denamur, E
通讯作者：
Denamur, E
影响因子：
--
作者：
Abe, Cecilia M.;Salvador, Fabia A.;Gomes, Tania A. T.
通讯作者：
Gomes, Tania A. T.
影响因子：
4
作者：
Bettelheim, KA;Kuzevski, A;McSweeney, CS
通讯作者：
McSweeney, CS