Modulation of Shigella virulence in response to available oxygen in vivo.
Modulation of Shigella virulence in response to available oxygen in vivo.
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作者：
细菌协调表达毒力决定因素，以响应其宿主的局部微环境。在这里，我们表明引起痢疾的福氏志贺氏菌在胃肠道（GI）中遇到不同的氧浓度，这控制了其第三型分泌系统（T3SS）的活性；T3SS对细胞侵袭和毒力至关重要。在厌氧环境中（如胃肠道腔），志贺氏菌表达延伸的T3SS针，同时减少入侵质粒抗原（Ipa）效应物的分泌。这是由FNR介导的，FNR是一种无氧代谢调节剂，可以抑制spa32和spa33的转录，而spa32和spa33是通过T3SS调节分泌的毒力基因。我们证明了在胃肠道粘膜附近有一个相对氧合区，这是由绒毛尖端的毛细血管网络扩散引起的。这将逆转Ipa分泌的厌氧阻断，允许T3SS在其精确的作用位点激活，增强入侵和毒力。
Bacteria co-ordinate expression of virulence determinants in response to localised microenvironments in their hosts. Here we show that Shigella flexneri, which causes dysentery, encounters varying oxygen concentrations in the gastrointestinal (GI) tract, which govern activity of its type three secretion system (T3SS); the T3SS is essential for cell invasion and virulence. In anaerobic environments (e.g. the GI tract lumen), Shigella expresses extended T3SS needles while reducing Ipa (Invasion plasmid antigen) effector secretion. This is mediated by FNR, a regulator of anaerobic metabolism that represses transcription of spa32 and spa33, virulence genes that the switch in secretion through the T3SS. We demonstrate there is a zone of relative oxygenation adjacent to the GI tract mucosa, caused by diffusing from the capillary network at the tips of villi. This would reverse the anaerobic block of Ipa secretion, allowing T3SS activation at its precise site of action, enhancing invasion and virulence.
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影响因子：
3.1
作者：
Bahrani, FK;Sansonetti, PJ;Parsot, C
通讯作者：
Parsot, C
影响因子：
3.4
作者：
Melican, Keira;Boekel, Jorrit;Richter-Dahlfors, Agneta
通讯作者：
Richter-Dahlfors, Agneta
影响因子：
6.7
作者：
Pentecost, Mickey;Otto, Glen;Theriot, Julie A;Amieva, Manuel R
通讯作者：
Amieva, Manuel R
影响因子：
3.2
作者：
Becker, S;Holighaus, G;Unden, G
通讯作者：
Unden, G
影响因子：
64.8
作者：
Maxwell, PH;Wiesener, MS;Ratcliffe, PJ
通讯作者：
Ratcliffe, PJ