Two-component system UhpAB facilitates the pathogenicity of avian pathogenic <i>Escherichia coli</i> through biofilm formation and stress responses
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Avian pathogenic <i>Escherichia coli</i> (APEC) is an important zoonotic pathogen that infects avian species by colonizing the gastrointestinal, respiratory, or reproductive tracts, leading to significant economic losses to the poultry industry worldwide and threatening food security and human health. APEC has evolved the two-component signal transduction system (TCS) to adapt and respond to extracellular environmental stresses, which are produced when the host is invaded by APEC. Here, we focus on the effect of the UhpAB TCS on the pathogenicity of APEC. The results in this study showed that the UhpAB TCS contributed to the pathogenicity of APEC in a chicken infection model. The electrophoretic mobility shift assays (EMSA) confirmed that UhpAB specifically bound to the promoters of <i>fepG</i>, <i>ldrD</i>, <i>ycgV</i>, and <i>ydeI</i>, and activated their expression, measured using real-time reverse transcription PCR (real-time RT–PCR). Furthermore, the UhpAB TCS could promote biofilm formation by activating the expression of biofilm master transcriptional regulator encoding gene <i>csgD</i> and enhance stress tolerance by activating the expression of stress protein encoding genes <i>uspA</i> and <i>bhsA</i>, thereby assisting APEC to evade host immune responses and inflammatory responses, and increasing the pathogenicity of APEC. These findings deepen our understanding of the pathogenic mechanism in APEC and offer new perspectives for further studies on the prevention and control of APEC infection. <b>RESEARCH HIGHLIGHTS</b>UhpAB increases the pathogenicity of APEC.UhpAB activates the expression of virulence genes <i>fepG</i>, <i>ldrD</i>, <i>ycgV</i>, and <i>ydeI</i>.UhpAB promotes biofilm formation and enhances stress tolerance.UhpAB contributes to APEC evading attack by the host immune system. UhpAB increases the pathogenicity of APEC. UhpAB activates the expression of virulence genes <i>fepG</i>, <i>ldrD</i>, <i>ycgV</i>, and <i>ydeI</i>. UhpAB promotes biofilm formation and enhances stress tolerance. UhpAB contributes to APEC evading attack by the host immune system.
禽致病性大肠杆菌（Avian pathogenic Escherichia coli, APEC）是一类重要的人畜共患病原体，可通过定殖禽类的胃肠道、呼吸道或生殖道实现感染，给全球家禽养殖业造成重大经济损失，同时威胁粮食安全与人类健康。APEC进化出双组分信号转导系统（two-component signal transduction system, TCS）以适应并响应宿主入侵时产生的胞外环境胁迫。本研究聚焦UhpAB TCS对APEC致病性的影响。研究结果显示，在鸡感染模型中，UhpAB TCS可增强APEC的致病性。电泳迁移率变动分析（electrophoretic mobility shift assays, EMSA）证实，UhpAB可特异性结合fepG、ldrD、ycgV以及ydeI的启动子区域，并通过实时逆转录聚合酶链式反应（real-time reverse transcription PCR, real-time RT–PCR）验证其可激活上述基因的表达。进一步研究发现，UhpAB TCS可通过激活生物膜主要转录调控因子编码基因csgD的表达促进生物膜形成，并通过激活应激蛋白编码基因uspA与bhsA的表达增强应激耐受性，进而帮助APEC逃避免疫宿主的免疫应答与炎症反应，提升其致病性。本研究加深了学界对APEC致病机制的理解，为APEC感染的防控研究提供了全新视角。 **研究亮点** UhpAB可增强APEC的致病性。 UhpAB可激活毒力基因fepG、ldrD、ycgV及ydeI的表达。 UhpAB可促进生物膜形成并增强应激耐受性。 UhpAB可助力APEC逃避免疫宿主的免疫系统攻击。 UhpAB可增强APEC的致病性。 UhpAB可激活毒力基因fepG、ldrD、ycgV及ydeI的表达。 UhpAB可促进生物膜形成并增强应激耐受性。 UhpAB可助力APEC逃避免疫宿主的免疫系统攻击。
