Affiliations: Institute of Genetic Engineering and Biotechnology, University of Baghdad, Baghdad, Iraq
Correspondence:
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Corresponding author: Halah Ahmed Abdulqader, Institute of Genetic Engineering and Biotechnology, University of Baghdad, Baghdad, Iraq. E-mail: zainab.h@ige.uobaghdad.edu.iq.
Abstract: BACKGROUND:Staphylococcus hominis is an opportunistic pathogen that expresses surface proteins, which are adhesive proteins that play a major role in biofilm formation. Biofilm is a protective layer that provides S. hominis bacteria with greater antibiotic resistance and promotes its adherence to biomedical surfaces, facilitating its entry into the bloodstream. OBJECTIVE: This research aimed to investigate the activity of Salicylic Acid (SA) and its effect on the gene expression of biofilm genes (FnbA and FnbB genes). METHODS: A total of 150 blood specimens were collected from patients. The specimens were cultured in broth media of the BacT/ALERT® system and subcultured on blood and chocolate agar. Bacteria were detected using the VITEK2 system. FnbA and FnbB genes were detected using PCR. The broth microdilution method performed the minimum inhibitory concentration (MIC) of Salicylic acid (SA) on S. hominis isolates with both genes. Detection of the gene expression levels of FnbA and FnbB genes was assessed using Real-Time PCR(RT-PCR). RESULTS: The results showed that out of the 150 specimens collected, 35 were S. hominis. The detection of S. hominis bacteria was performed by PCR amplification of two genes FnbA and FnbB and showed 100% and 17.14% of isolates were positive for genes FnbA and FnbB, respectively. The expression of FnbA and FnbB genes was decreased in samples treated with SA compared with untreated ones. CONCLUSION: In conclusion, there is a significant impact of SA on the prevention of biofilm formation of S. hominis through the suppression of gene expression, specifically FnbA and FnbB. This could enhance susceptibility to antimicrobial treatments. However, more research is required to determine whether SA leads to the selection of resistant bacteria.
