Potential Role of SdiA in Biofilm Formation and Drug Resistance in Avian Pathogenic Escherichia coli.

Simple Summary: Avian pathogenic Escherichia coli (APEC) constitutes a notable etiological agent of colibacillosis, an inflammatory disease in birds that leads to considerable economic losses within the poultry industry. In this study, we probed into the impact of the quorum sensing regulator SdiA on the transcriptional profiling of an APEC strain and proved the potential regulatory role of SdiA in biofilm formation, motility, and drug resistance. The discoveries disclose the involvement of SdiA in the pathogenesis of APEC and will furnish some novel insights into the prevention and control of colibacillosis induced by APEC. Avian pathogenic Escherichia coli (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 Escherichia coli, 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 sdiA 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 t-test were conducted on the datasets. This research confirmed that SdiA inhibits biofilm formation by 1.9-fold (p-value < 0.01) and motility by 1.5-fold (p-value < 0.01). RT-qPCR revealed that SdiA positively regulates multidrug resistance by upregulating the expression of yafP, cbrA, and eamB. Collectively, the results of this study indicate the role of SdiA in the pathogenesis of APEC by controlling biofilm formation, motility, and multidrug resistance. [ABSTRACT FROM AUTHOR]