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首页> 外文期刊>Pathogens >Histone Deacetylase 6 Regulates Bladder Architecture and Host Susceptibility to Uropathogenic Escherichia coli
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Histone Deacetylase 6 Regulates Bladder Architecture and Host Susceptibility to Uropathogenic Escherichia coli

机译：组蛋白脱乙酰基酶6调节膀胱结构和宿主对致病性大肠杆菌的敏感性

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Histone deacetylase 6 (HDAC6) is a non-canonical, mostly cytosolic histone deacetylase that has a variety of interacting partners and substrates. Previous work using cell-culture based assays coupled with pharmacological inhibitors and gene-silencing approaches indicated that HDAC6 promotes the actin- and microtubule-dependent invasion of host cells by uropathogenic Escherichia coli (UPEC). These facultative intracellular pathogens are the major cause of urinary tract infections. Here, we examined the involvement of HDAC6 in bladder colonization by UPEC using HDAC6 knockout mice. Though UPEC was unable to invade HDAC6 ?/? cells in culture, the bacteria had an enhanced ability to colonize the bladders of mice that lacked HDAC6. This effect was transient, and by six hours post-inoculation bacterial titers in the HDAC6 ?/? mice were reduced to levels seen in wild type control animals. Subsequent analyses revealed that the mutant mice had greater bladder volume capacity and fluid retention, along with much higher levels of acetylated a-tubulin. In addition, infiltrating neutrophils recovered from the HDAC6 ?/? bladder harbored significantly more viable bacteria than their wild type counterparts. Cumulatively, these changes may negate any inhibitory effects that the lack of HDAC6 has on UPEC entry into individual host cells, and suggest roles for HDAC6 in other urological disorders such as urinary retention.
机译：组蛋白脱乙酰基酶6（HDAC6）是非规范的，主要是胞质组蛋白脱乙酰基酶，具有多种相互作用的伴侣和底物。以前使用基于细胞培养的分析方法结合药理学抑制剂和基因沉默方法进行的研究表明，HDAC6促进尿毒症性大肠杆菌（UPEC）对肌动蛋白和微管依赖性宿主细胞的侵袭。这些兼性的细胞内病原体是尿路感染的主要原因。在这里，我们使用HDAC6基因敲除小鼠研究了UPEC在HDAC6膀胱定植中的作用。尽管UPEC无法入侵HDAC6？在培养细胞中，这种细菌具有增强的能力，可以在缺少HDAC6的小鼠的膀胱中定植。这种作用是暂时的，并且在接种后六小时内HDAC6β/β中的细菌滴度较高。将小鼠降低到在野生型对照动物中看到的水平。随后的分析表明，突变小鼠具有更大的膀胱容量和液体滞留能力，以及更高水平的乙酰化α-微管蛋白。另外，从HDAC6α/β中回收的浸润中性粒细胞。膀胱中所含的细菌比野生型细菌要多得多。累积地，这些变化可以消除缺乏HDAC6对UPEC进入单个宿主细胞的任何抑制作用，并暗示HDAC6在其他泌尿系统疾病（如尿retention留）中的作用。

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