LitR of Vibrio salmonicida Is a Salinity-Sensitive Quorum-Sensing Regulator of Phenotypes Involved in Host Interactions and Virulence

• Published in: Infection and Immunity
• Main Authors: Bjelland, Ane Mohn, Sørum, Henning, Tegegne, Daget Ayana, Winther-Larsen, Hanne C., Willassen, Nils Peder, Hansen, Hilde
• Format: Text
• Language: English
• Published: American Society for Microbiology 2012
• Subjects: Cellular Microbiology: Pathogen-Host Cell Molecular Interactions; Atlantic salmon
• Online Access: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3347430; http://www.ncbi.nlm.nih.gov/pubmed/22371373; https://doi.org/10.1128/IAI.06038-11

Vibrio (Aliivibrio) salmonicida is the causal agent of cold-water vibriosis, a fatal bacterial septicemia primarily of farmed salmonid fish. The molecular mechanisms of invasion, colonization, and growth of V. salmonicida in the host are still largely unknown, and few virulence factors have been identified. Quorum sensing (QS) is a cell-to-cell communication system known to regulate virulence and other activities in several bacterial species. The genome of V. salmonicida LFI1238 encodes products presumably involved in several QS systems. In this study, the gene encoding LitR, a homolog of the master regulator of QS in V. fischeri, was deleted. Compared to the parental strain, the litR mutant showed increased motility, adhesion, cell-to-cell aggregation, and biofilm formation. Furthermore, the litR mutant produced less cryptic bioluminescence, whereas production of acylhomoserine lactones was unaffected. Our results also indicate a salinity-sensitive regulation of LitR. Finally, reduced mortality was observed in Atlantic salmon infected with the litR mutant, implying that the fish were more susceptible to infection with the wild type than with the mutant strain. We hypothesize that LitR inhibits biofilm formation and favors planktonic growth, with the latter being more adapted for pathogenesis in the fish host.