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Updated: Jun 30, 2026

Biosensor for Detection of Antibiotic Resistant Staphylococcus Bacteria
Published on: May 8, 2013
Expression of cell surface markers on methicillin resistant Staphylococcus aureus stimulated lymphocytes
Isil Fidan1, Emine Yesilyurt, Berna Erdal
1Gazi University, Faculty of Medicine, Department of Medical Microbiology, Ankara, Turkey. isilfidan@yahoo.com
Background & Objective:
Methicillin-resistant Staphylococcus aureus (MRSA) has gradually been increasing, new strategies in the treatment of MRSA infections are required. This depends on the understanding of the infection pathogenesis and the immune response. This study was therefore designed to determine the immune response which develops during MRSA infection and the role of chemokines in this response, and also to compare the results with the changes occurring after MSSA infection.
Methods:
The expression of the surface markers of human lymphocytes stimulated by heat-killed MRSA or MSSA was analysed by flow cytometry. The chemokine levels in the lymphocytes culture supernatants stimulated or not stimulated by microorganisms were determined by ELISA.
Results:
Human peripheral blood mononuclear cells (PBMCs) stimulated by MRSA the levels of CD4(+)CD25(+) regulatory T cells, CD69 expressions in the activated T lymphocytes, CD3(-)CD16(+)CD56(+) NK cells and the levels of MIP-1alpha, MIP-1beta, MCP-1 chemokines increased as compared to the cells not stimulated by MRSA. Although stimulation by MSSA caused an increase in CD25 expression after 24 h, the increase was found to be lower than the one caused by MRSA stimulation. The increase in CD69 expression was statistically significant compared to the cells stimulated by MRSA. Different from the cells stimulated by MRSA, no change was observed in the expressions of CD54 and CD3(-)CD16(+)CD56(+) NK cells in the cells stimulated by MSSA.
Interpretation & Conclusion:
Our findings showed that cellular as well as humoral immunity are critical in MRSA infection and that T cell activation and the increase in chemokines may play a role in the regulation of immune response.
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