The Role of luxS in Histophilus somni Virulence and Biofilm Formation

Abstract

S-ribosylhomocysteinase (LuxS) is required for the synthesis of the autoinducer-2 (AI-2) quorum-sensing signalling molecule in many Gram-negative bacteria. The bovine (and ovine) opportunistic pathogen Histophilus somni contains a luxS, and forms a biofilm containing an exopolysaccharide (EPS) in the matrix. Since biofilm formation is regulated by quorum sensing in many bacteria, the role of luxS in H. somni virulence and biofilm formation was investigated. Although culture supernatants from H. somni were ineffective at inducing bioluminescence in the Vibrio harveyi reporter strain BB170, H. somni luxS complemented the biosynthesis of AI-2 in the luxS-deficient Escherichia coli strain DH5α. H. somni strain 2336 luxS was inactivated by tranposon mutagenesis. Comparison of RNA exression profiles revealed that many genes were significantly differentially expressed in the luxS mutant compared to the wildtype, whether the bacteria were grown planktonically or in a biofilm. Furthermore, the luxS mutant had a truncated and asialylated lipooligosaccharide (LOS), and was substantially more serum-sensitive than the wildtype. Not surprisingly, the luxS mutant was attenuated in a mouse model for H. somni virulence, and some of the altered phenotypes were partially restored after the mutation was complemented with a functional luxS. However, no major differences were observed between the wildtype and the luxS mutant in regard to outer membrane protein profiles, biofilm formation, EPS production, or intracellular survival. These results indicate that luxS plays a role in H. somni virulence in the context of LOS biosynthesis, but not biofilm formation or other phenotypic properties examined.

Effects of chlorogenic acid on antimicrobial, antivirulence, and anti-quorum sensing of carbapenem-resistant Klebsiella pneumoniae

“…Furthermore, Balestrino et al (2005) revealed that the luxS mutant could form a mature biofilm but one that had reduced capacity to develop microcolonies, mostly in the early steps of the biofilm formation, indicting the deletion of QS genes may not influence biofilm formation. Pan et al (2021) found that no major differences were observed between the wild-type and the luxS mutant in regard to outer membrane protein profiles, biofilm formation, exopoly saccharides (EPS) production, or intracellular survival, which indicating that the deletion of QS genes may not reduce biofilm formation. The genes of mrkA , wzm , wbbm , and treC are all involved in the biofilm formation of K. pneumoniae ( Vuotto et al, 2017 ), wzm and wbbM are lipopolysaccharide (LPS) synthesis-related genes and participate in LPS production.…”

1,8-Cineole inhibits biofilm formation and bacterial pathogenicity by suppressing luxS gene expression in Escherichia coli

“…Previous studies have demonstrated that the luxS gene could regulate bacterial pathogenicity. The deletion of luxS gene in Histophilus somni significantly affected the pathogenicity of the bacteria in mice ( Pan, Siddaramappa et al, 2021 ). The 50% lethal dose (LD50) of the E. piscicida ΔluxS strain for zebrafish was significantly higher than that of the wild-type strain, which suggests that the luxS gene deletion could attenuate virulence of E. piscicida ( Sun, Li et al, 2020 ).…”