Th1-Th17 cells contribute to the development of uropathogenic Escherichia coli-induced chronic pelvic pain.

Th1-Th17 cells contribute to the development of uropathogenic Escherichia coli-induced chronic pelvic pain.
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Th1-Th17 细胞有助于尿路致病性大肠杆菌引起的慢性盆腔疼痛的发生。

DOI:
10.1371/journal.pone.0060987
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Thumbikat P
Thumbikat P
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Quick ML;Wong L;Mukherjee S;Done JD;Schaeffer AJ;Thumbikat P

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男性慢性前列腺炎/慢性盆腔疼痛综合征的病因不明,但可能涉及微生物和自身免疫机制。我们用慢性盆腔疼痛患者的临床大肠杆菌分离物(CP-1)建立了NOD/ShiLtJ (NOD)小鼠慢性盆腔疼痛感染模型。我们研究了NOD小鼠的疼痛机制,并将其与C57BL/6 (B6)小鼠进行了比较,C57BL/6是一种抗cp -1诱导疼痛的品系。从cp -1感染的NOD小鼠中过继转移CD4+ T细胞,而不是血清,足以诱导慢性盆腔疼痛。cp -1感染NOD小鼠的CD4+ T细胞表达IFN-γ和IL-17A,但不表达IL-4,与Th1/Th17免疫特征一致。体外扩增的IFN-γ或il - 17a表达细胞的过继转移足以诱导naïve NOD受体的盆腔疼痛。NOD-IFN-γ-KO小鼠盆腔疼痛并未消除,但与CP1感染的IL-17A免疫反应增强有关。这些发现证明了Th1和th17介导的适应性免疫机制在慢性盆腔疼痛中的新作用。
The etiology of chronic prostatitis/chronic pelvic pain syndrome in men is unknown but may involve microbes and autoimmune mechanisms. We developed an infection model of chronic pelvic pain in NOD/ShiLtJ (NOD) mice with a clinical Escherichia coli isolate (CP-1) from a patient with chronic pelvic pain. We investigated pain mechanisms in NOD mice and compared it to C57BL/6 (B6) mice, a strain resistant to CP-1-induced pain. Adoptive transfer of CD4+ T cells, but not serum, from CP-1-infected NOD mice was sufficient to induce chronic pelvic pain. CD4+ T cells in CP-1-infected NOD mice expressed IFN-γ and IL-17A but not IL-4, consistent with a Th1/Th17 immune signature. Adoptive transfer of ex-vivo expanded IFN-γ or IL-17A-expressing cells was sufficient to induce pelvic pain in naïve NOD recipients. Pelvic pain was not abolished in NOD-IFN-γ-KO mice but was associated with an enhanced IL-17A immune response to CP1 infection. These findings demonstrate a novel role for Th1 and Th17-mediated adaptive immune mechanisms in chronic pelvic pain.
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发表时间: 2009-07-01
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