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<p>Avian Pathogenic <i>Escherichia coli</i> (APEC) is a major causative agent of colibacillosis, a severe respiratory disease in birds that leads to significant economic losses in poultry production industry. The two-component systems (TCSs) CitA/CitB regulates metabolism and stress adaptation in <i>Enterobacteriaceae</i>, but its contribution to virulence, particularly in APEC, is undefined. In this study, we investigated the function of the CitA/CitB in APEC by analyzing the transcriptional profile of wild-type strain APEC40 compared to a <i>citAB</i>-deletion mutant. Microarray analysis revealed that CitA/CitB significantly impacts the transcription of numerous genes, including multiple genes associated with biofilm formation and virulence. Phenotypic assays confirmed that inactivation of <i>citAB</i> significantly enhanced biofilm formation capacity and multidrug resistance. Quantitative real-time PCR (qRT-PCR) analysis demonstrated that CitAB negatively regulates expression of key genes involved in these phenotypes, including <i>mglB</i>, <i>fimB</i>, <i>glcB</i>, <i>mblC</i>, <i>ompC</i>, <i>ompW</i>, and <i>pgaB</i>. Collectively, these results demonstrate that the CitA/CitB acts as a negative regulator of biofilm formation, multidrug resistance, and key virulence-associated genes in APEC.</p>

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The CitAB two-component system is involved in pathogenesis regulation in Avian pathogenic Escherichia coli

  • 期刊论文

  • 发表日期：

    2025年9月12日

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  • Zhuo Cheng,
  • Yuhang Chen,
  • Kai Ma,
  • Yiqian Yang,
  • Hao Pei,
  • Mei Yu,
  • Fei Shang

摘要

Avian Pathogenic Escherichia coli (APEC) is a major causative agent of colibacillosis, a severe respiratory disease in birds that leads to significant economic losses in poultry production industry. The two-component systems (TCSs) CitA/CitB regulates metabolism and stress adaptation in Enterobacteriaceae, but its contribution to virulence, particularly in APEC, is undefined. In this study, we investigated the function of the CitA/CitB in APEC by analyzing the transcriptional profile of wild-type strain APEC40 compared to a citAB-deletion mutant. Microarray analysis revealed that CitA/CitB significantly impacts the transcription of numerous genes, including multiple genes associated with biofilm formation and virulence. Phenotypic assays confirmed that inactivation of citAB significantly enhanced biofilm formation capacity and multidrug resistance. Quantitative real-time PCR (qRT-PCR) analysis demonstrated that CitAB negatively regulates expression of key genes involved in these phenotypes, including mglB, fimB, glcB, mblC, ompC, ompW, and pgaB. Collectively, these results demonstrate that the CitA/CitB acts as a negative regulator of biofilm formation, multidrug resistance, and key virulence-associated genes in APEC.