SesI May Be Associated with the Invasiveness of Staphylococcus epidermidis
Xiuqin Qi1, Ye Jin1, Jingjing Duan1
1Department of Clinical Laboratory, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Abstract:
Staphylococcus epidermidis is a commensal bacterium which widely colonizes in human skin and mucous membrane and rarely causes clinically manifested infections. S. epidermidis surface protein I (SesI) is considered to be the major virulence factor of S. epidermidis infection, but its pathogenesis is not clear. Here, we demonstrated that the prevalence of sesI among S. epidermidis invasive isolates (20.8%, 26/125) was significantly higher than that among colonizing isolates (3.8%, 4/106). The positive rates of biofilm-associated genes (aap, icaA, IS256) and resistance-associated genes mupA among the sesI-positive isolates were significantly higher than those among sesI-negative isolates (p < 0.05). And antimicrobial susceptibility testing showed that the resistance rates of sesI-positive isolates to ciprofloxacin, gentamicin and trimethoprim/sulfamethoxazole were significantly higher than those among sesI-negative isolates. Interestingly, 80.8% (21/26) of sesI-positive isolates belong to ST2 determined by MLST, while ST2 was not found among any of the 99 sesI-negative invasive isolates, indicating that there is a strong association between carriage of sesI and ST2 clone. In order to further study the role of sesI gene in pathogenesis, the sesI gene mutant (S. epidermidis RP62AΔsesI) and complementary expression strain (S. epidermidis RP62AΔsesI-C) were successfully constructed. All experimental data indicated that sesI may promote S. epidermidis to adhere and aggregate, but it had no obvious effect on the mature stage of biofilm formation. Taken together, these results suggest that sesI, along with antimicrobial and other biofilm-associated genes enables S. epidermidis easier for colonization and adhesion and contributes to the spread of S. epidermidis, especially ST2 clone.
Insights
Staphylococcus epidermidis surface protein I (SesI) promotes bacterial adhesion and aggregation, particularly in the ST2 clone. This virulence factor is linked to increased antimicrobial resistance and biofilm gene prevalence in invasive strains.
Area of Science:
- Microbiology
- Infectious Diseases
- Molecular Biology
Background:
- Staphylococcus epidermidis is a common skin bacterium that can cause infections.
- The role of its surface protein I (SesI) in pathogenesis is not well understood.
Purpose of the Study:
- To investigate the prevalence and role of the sesI gene in S. epidermidis virulence.
- To determine the association of sesI with antimicrobial resistance and biofilm formation.
Main Methods:
- Prevalence study of sesI in invasive and colonizing S. epidermidis isolates.
- Analysis of biofilm-associated and antimicrobial resistance genes.
- Antimicrobial susceptibility testing.
- Multilocus sequence typing (MLST) to identify sequence types (STs).
- Construction of sesI gene mutant and complementary strains.
Main Results:
- The sesI gene was significantly more prevalent in invasive (20.8%) than colonizing (3.8%) S. epidermidis isolates.
- SesI-positive isolates showed higher rates of biofilm-associated genes (aap, icaA, IS256) and the mupA resistance gene.
- SesI-positive isolates exhibited increased resistance to ciprofloxacin, gentamicin, and trimethoprim/sulfamethoxazole.
- A strong association was found between sesI carriage and the ST2 clone (80.8% of sesI-positive isolates).
- Experimental data suggested sesI promotes S. epidermidis adhesion and aggregation but not mature biofilm formation.
Conclusions:
- The sesI gene is associated with increased virulence, antimicrobial resistance, and specific clones (ST2) of S. epidermidis.
- SesI likely contributes to bacterial colonization and adhesion, facilitating the spread of S. epidermidis infections.
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