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首页> 外文期刊>Cell and Tissue Research >Systemic LPS induces toll-like receptor 3 (TLR3) expression and apoptosis in testicular mouse tissue
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Systemic LPS induces toll-like receptor 3 (TLR3) expression and apoptosis in testicular mouse tissue

机译：全身LPS在睾丸组织中诱导有收缩的受体3（TLR3）表达和凋亡

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It is well known that sepsis and inflammation reduce male fertility. Within the testis, toll-like receptor 3 (TLR3) is constitutively expressed and recognizes double-stranded RNA (dsRNA) from viruses, degraded bacteria, damaged tissues and necrotic cells. To characterize the potential role of TLR3 in response to testicular infections, its expression and downstream signaling were investigated upon challenge with lipopolysaccharides (LPS) in two mouse strains that differ in their immuno-competence regarding T cell-regulated immunity. Thereto, Balb/c and Foxn1nu mice were randomized into six interventional groups treated with either i.v. application of saline or LPS followed by 20 min, 5 h 30 min and 18 h of observation and two sham-treated control groups. LPS administration induced a significant stress response; the amplification was manifested for TLR3 and interleukin 6 (IL6) mRNA in the impaired testis 5 h 30 min after LPS injection. TLR3 immunostaining revealed that TLR3 was primarily localized in spermatocytes. The TLR3 expression displayed different temporal dynamics between both mouse strains. However, immunofluorescence staining indicated only punctual interferon regulatory factor 3 (IRF3) expression upon LPS treatment along with minor alterations in interferon beta (IFN beta) mRNA expression. Induction of acute inflammation was closely followed by a significant shift of the Bax/Bcl2 ratio to pro-apoptotic signaling accompanied by augmented TUNEL-positive cells 18 h after LPS injection with again differing patterns in both mouse strains. In conclusion, this study shows the involvement of TLR3 in response to LPS-induced testicular inflammation in immuno-competent and -incompetent mice, yet lacking transmission into its signaling pathway.
机译：众所周知，败血症和炎症可降低雄性生育率。在睾丸内，组成思考的受体3（TLR3），并识别来自病毒，降解细菌，受损组织和坏死细胞的双链RNA（DSRNA）。为了表征TLR3响应于睾丸感染的潜在作用，在脂多糖（LPS）攻击两种小鼠菌株的攻击时，研究其表达和下游信号在其免疫能力方面有关T细胞调节的免疫力。其中，Balb / c和Foxn1nu小鼠随机分为六个介入组，用I.v.盐水或LPS的施用，然后施加20分钟，5小时30分钟和18小时，观察和两个假处理的对照组。 LPS管理诱导显着的压力反应;在LPS注射后30分钟，将扩增的TLR3和白细胞介素6（IL6）mRNA中显示为TLR3和白细胞介素6（IL6）mRNA。 TLR3免疫染色显示TLR3主要局限于精子细胞。 TLR3表达式显示两个鼠标菌株之间的不同时间动态。然而，免疫荧光染色仅表明在LPS处理中仅在LPS处理时表达，以及干扰素β（IFNβ）mRNA表达的微小改变。急性炎症的诱导是紧密的，然后在LPS注射后伴有增强的TUNEL阳性细胞伴有增强的TUNEL-阳性细胞的促凋亡信号传递的显着变化，再次在两种小鼠菌株中再次不同图案。总之，本研究表明，TLR3响应于LPS诱导的免疫竞争力和 - 耐受小鼠的睾丸炎症，但缺乏传输到其信号通路。

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