Expression of cell surface markers on methicillin resistant Staphylococcus aureus stimulated lymphocytes.

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.

The effects of fluconazole and cytokines on human mononuclear cells

Candida infections are common infections and fluconazole is one of the most frequently administered antifungal agents in their treatment. The resistance developed against antifungal agents has necessitated the improvement of new treatments. This study focuses on the investigation of the effect of fluconazole and cytokines such as interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF) on chemokine production and anticandidal activity of human monocytes. In the study it was observed that GM-CSF caused an increase in candidacidal activity of monocytes. Anticandidal activity of GM-CSF + IFN-gamma combination was not found to be more effective than GM-CSF or IFN-gamma alone. The presence of cytokine and fluconazole caused an increase in the levels of CCL3 and CCL4 chemokines. Accordingly, it was considered that chemokines could contribute to the efficacy of fluconazole in C. albicans infections. Besides, in order to strengthen the immune system some cytokines might be used in addition to antifungal agents for the treatment.

Evaluation of the natural killer cytotoxicity and the levels of cytokines in rats with type I diabetes mellitus

Type I diabetes mellitus (insulin-dependent DM = IDDM) is a chronic disease characterized by specific destruction of pancreatic beta cells, resulting in an absolute lack of insulin. Immune mechanisms, genetic susceptibility, and environmental factors are all implicated in the pathogenesis of Type 1 diabetes. This study was aimed at determining the efficiency of cytokines, natural killer (NK) cells in the pathophysiology of IDDM. Therefore, we evaluated the plasma levels of cytokines by specific enzyme-linked immunosorbent assay (ELISA) and the cytotoxicity activity of NK cells by anti-candididal index in rats with type I diabetes. We found that the cytotoxicity activity of NK cells in IDDM groups significantly decreased compared to the control groups. The levels of interferon-g (IFN-g) in IDDM groups were slightly higher than in healthy controls. These results indicate that the changes of T H1 type cytokines such as IFN-g and NK cell activity can play a role in the etiology of IDDM. The data may provide new strategies for the treatment of IDDM.