Regulatory effects on virulence and phage susceptibility revealed by mutation in .

INTRODUCTION

The World Health Organization has identified multi-drug resistant strains as the highest priority in 2024. Understanding the regulatory routes of virulence features is crucial for the development of novel anti-virulence strategies. SdiA, a LuxR-like quorum sensing (QS) receptor that responds to acyl-homoserine lactones (AHLs), is involved in the regulation of virulence traits in some Gram-negative bacteria. The function of this receptor in the virulence of remains uncertain. The objective of the present study was to elucidate the function of SdiA in biofilm formation and virulence.

METHODS

To this end, a genetic knockout of was conducted, and virulence-related phenotypic studies were performed following AHL provision.

RESULTS AND DISCUSSION

The results demonstrate that deficiency increases susceptibility to phage infection and human serum resistance, and promotes biofilm maturation and cell filamentation, although no effect on virulence was observed in the infection model. On the other hand, C6-HSL promoted -dependent biofilm maturation, capsule production and serum resistance while reducing virulence against in the absence of . The addition of C6-HSL did not affect phage susceptibility. The results of this study demonstrate that AHLs and SdiA exert a dual influence on virulence phenotypes, operating both independently and hierarchically. These findings provide new insights into the virulence of and its regulation by SdiA.