Hai Haowen, Yang Mengyang, Cheng Zhuo, Ma Kai, Shang Fei
School of Life Sciences, Anhui Agricultural University, Hefei 230036, China.
Animals (Basel). 2024 Jul 28;14(15):2199. doi: 10.3390/ani14152199.
Avian pathogenic (APEC) constitutes a significant cause of colibacillosis, a localized or systemic inflammatory disorder in avian species, resulting in considerable economic losses within the global poultry industry. SdiA (suppressor of division inhibitor) is a transcription factor recognized as a LuxR homolog in , regulating various behaviors, including biofilm formation, multidrug resistance, and the secretion of virulence factors. However, the function of SdiA in APEC strains and its correlation with virulence and multidrug resistance remains unknown. This study probed into the function of SdiA by analyzing the effect of deletion on the transcription profile of an APEC strain. The microarray data revealed that SdiA upregulates 160 genes and downregulates 59 genes, exerting a particularly remarkable influence on the transcription of multiple virulence genes. A series of antibiotic sensitivity tests, biofilm formation assays, motility assays, and transcriptome analyses were performed, while a Normality test and -test were conducted on the datasets. This research confirmed that SdiA inhibits biofilm formation by 1.9-fold (-value < 0.01) and motility by 1.5-fold (-value < 0.01). RT-qPCR revealed that SdiA positively regulates multidrug resistance by upregulating the expression of , , and . Collectively, the results of this study indicate the role of SdiA in the pathogenesis of APEC by controlling biofilm formation, motility, and multidrug resistance.
禽致病性大肠杆菌(APEC)是禽大肠杆菌病的一个重要病因,禽大肠杆菌病是禽类的一种局部或全身性炎症性疾病,给全球家禽业造成了相当大的经济损失。SdiA(分裂抑制因子的抑制因子)是一种转录因子,在大肠杆菌中被认为是LuxR同系物,它调节多种行为,包括生物膜形成、多药耐药性和毒力因子的分泌。然而,SdiA在APEC菌株中的功能及其与毒力和多药耐药性的关系尚不清楚。本研究通过分析缺失SdiA对一株APEC菌株转录谱的影响,探讨了SdiA的功能。微阵列数据显示,SdiA上调160个基因,下调59个基因,对多个毒力基因的转录产生了特别显著的影响。进行了一系列抗生素敏感性试验、生物膜形成试验、运动性试验和转录组分析,同时对数据集进行了正态性检验和t检验。本研究证实,SdiA可使生物膜形成减少1.9倍(P值<0.01),运动性降低1.5倍(P值<0.01)。RT-qPCR显示,SdiA通过上调mdtA、mdtB和mdtC的表达来正向调节多药耐药性。总的来说,本研究结果表明SdiA通过控制生物膜形成、运动性和多药耐药性在APEC发病机制中发挥作用。