DOI: 10.57760/sciencedb.25889
title: Characterization and immunoprotection of thioredoxin reductase TrxB knockout mutant of Salmonella Enteritidis
title: Characterization and immunoprotection of thioredoxin reductase TrxB knockout mutant of Salmonella Enteritidis

description:  Background: Salmonella Enteritidis is an important zoonotic pathogen that poses a major threat to animals and human health. TrxB, as a key component of the thioredoxin system, is a thioredoxin reductase ubiquitously present in organisms, mainly involved in maintaining cellular redox balance, but its role in the pathogenicity of S. Enteritidis remains unclear. In this study, we generated a trxB-deficient strain of S. Enteritidis C50336 strain to investigate how trxB affects the biological characteristics and pathogenesis of the bacterium. Results: We found that TrxB gene deletion didn't affect the growth and biochemical properties of the C50336 strain, but significantly reduced its motility, drug resistance, biofilm formation and tolerance to environmental stress. After TrxB knockout, the adhesion and invasion capacities of S. Enteritidis to Caco-2 cells, along with its proliferation ability in RAW264.7 cells, were significantly reduced. Additionally, the trxB-deficient strain exhibited significantly lower pathogenicity than the parental strain, evidenced by a more than 100-fold increase in LD50. The significant decrease of expression of virulence-related genes was also determinedd in the trxB-knockout mutant. More importantly, immunized mice with this deletion strain can confer a promising protection against the challenge of C50336 strain. Conclusion : These findings indicate that TrxB is a crucial virulence factor in S. Enteritidis, playing critical roles in its pathogenicity.
description:  Background: Salmonella Enteritidis is an important zoonotic pathogen that poses a major threat to animals and human health. TrxB, as a key component of the thioredoxin system, is a thioredoxin reductase ubiquitously present in organisms, mainly involved in maintaining cellular redox balance, but its role in the pathogenicity of S. Enteritidis remains unclear. In this study, we generated a trxB-deficient strain of S. Enteritidis C50336 strain to investigate how trxB affects the biological characteristics and pathogenesis of the bacterium. Results: We found that TrxB gene deletion didn't affect the growth and biochemical properties of the C50336 strain, but significantly reduced its motility, drug resistance, biofilm formation and tolerance to environmental stress. After TrxB knockout, the adhesion and invasion capacities of S. Enteritidis to Caco-2 cells, along with its proliferation ability in RAW264.7 cells, were significantly reduced. Additionally, the trxB-deficient strain exhibited significantly lower pathogenicity than the parental strain, evidenced by a more than 100-fold increase in LD50. The significant decrease of expression of virulence-related genes was also determinedd in the trxB-knockout mutant. More importantly, immunized mice with this deletion strain can confer a promising protection against the challenge of C50336 strain. Conclusion : These findings indicate that TrxB is a crucial virulence factor in S. Enteritidis, playing critical roles in its pathogenicity.