engleski

CHANGES ON CELL MEDIATED IMMUNITY OF PEOPLE SITUATED NEAR GASOLINE INDUSTRY

The majority of environmental diseases are multifactorial airway illnesses, including genetic background and exposure to different kind of airborne irritants and allergens. Altered lifestyle and changes in environmental exposures (such as: traffic emissions, cigarette smoke, photochemical smog components, industry irritants) contribute to the occurring of these diseases. Recent studies indicate that diesel exhaust particles act as adjuvant in the immune response and may lead to the enhancement of proinflammatory and proallergic response without exposure to allergen. The activities of diesel exhaust particles (DEPs) and volatile aromatic hydrocarbons (BTEX), may cause the increasing respiratory morbidity and mortality. Benzene is one of the most important air pollutants that are emitted by oil industry, since they are involved in almost every refinery process. Volatile organic compounds (BTEX) are major group of air pollutants and play a crucial role in ecological damages, disturbing the ecosystem and human health. The aim of the study: The immunological status of people situated near gasoline industry was the subject of our interest. It seems that cellular immunity is the most important way of host defense against environmental diseases. In this study we wanted to analyze the cytolitic activity of lymphocytes in peripheral blood of 30 subjects living along the oil industry and the same number of health donors. Cytotoxic lymphocytes or killer cells are the mediators in cell-mediated cytotoxicity (CMC) reactions. They comprise cytotoxic T lymphocytes (CTL) and natural killer (NK) cells. CTL are a part of the adoptive immune system and NK cells of the innate or natural immune system. Both CTL and NK cells are endowed with cytoplasmic granules containing the cytolytic molecule perforin and associated granule proteases. Perforin “perforates” target cell membranes by forming transmembrane pores, which lead to the equilibration of ionic gradients. Methods: In this study a flow cytometryc technique for detecting cytoplasmic perforin (P) has been used to quantify changes in peforin expression in human peripheral blood lymphocytes (PBL) of inhabitants leaving near gasoline industry, compared with health laboratory donors. Immunophenotypic profiles of perforin (P)-positive peripheral blood lymphocyte subsets were measured by simultaneous detection of P (intracellular antigen ; (FITC)-conjugated anti-perforin ) and cell-surface antigens (phycoerythrin (PE)-conjugated anti-CD 3, CD4, CD8, CD16 and CD56), (Becton Dickinson Co). All samples had adequate isotypic controls. Analysis was performed on flow cytometer (FACSCalibur, Becton Dickinson) using CELLQuestPro Software (Macintosh, Quadra 650). BTEX-analyze in urine, as an important method has also to be included in such kind of environmental monitoring. BTEX were analyzed from urine by a HS-SPME method which is similar as described I.Brčić-Karačonji and coauthors. The results were analyzed using the Sigma Plot for Windows, version 1.02. Statistical analyses were performed using a Student, s t-test one way analysis for comparison of means. All experiments have been approved by a local ethics committee. Results: Our data emphasized that the percentage of total perforin-positive cells in subjects living near gasoline industry is significantly decreased. Percentage of double positive cells (perforin positive and surface marker positive cells) was also decreased in all examined lymphocyte subpopulations. People living in urban industrial fields have significantly increased the concentration of benzene and toluene compared with our health laboratory donors. Conclusion: These results point that human perforin is differentially expressed in distinct sub-populations of peripheral blood lymphocytes of people exposure to gasoline and diesel, implicating the important role of perforin positive cells in naive immune response and cytotoxic activity of peripheral blood lymphocytes.

cell mediated immunity; environmental diseases; innate immunity; perforin

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