predictive value of HLA-DR matching and cytokine gene polymorphisms in renal allograft acute rejection: a living-unrelated donor [LURD] study

In addition to Human Leukocyte Antigens [HLA] compatibility, gene polymorphisms in cytokines might also be important in the quality of allogeneic immune response. To evaluate the influence of HLA-DR matching and a number of cytokine gene polymorphisms on acute rejection after living-unrelated donor [LURD] kidney transplantation. A total of 42 renal transplants performed at Hashemi Nejad Kidney Hospital [Tehran/Iran] and followed up for 3 months post-transplantation were included. Using PCR-SSP, HLA-DR alleles [DR1-18] of recipients and donors and gene polymorphisms in TNF-a, TGF-b1, IL-10, IL- 6, and IFN-g of recipients were determined. Acute rejection was observed in 11[26.2%] of renal recipients. The frequency of one and two HLA-DR mismatches in rejector group was 2[18.2%] and 9[81.8%] and in non-rejector group was 13[41.9%] and 17[54.8%], respectively. HLA-DR incompatibility was not significantly higher in rejector [1.82 +/- 0.40] compared with non-rejector [1.52 +/- 0.57] recipients [P=0.069] and more than half of non-rejectors had ompletely mismatched HLA-DR antigens with donors. Polymorphisms associated with the mentioned cytokines had no correlation with acute rejection. The predictive value of HLA-DR mismatching for acute rejection is not as prominent in LURD kidney transplantation as in the cadaveric one. In addition, we failed to demonstrate an association between combined cytokine genotypes and HLA-DR matching with acute rejection. Further and more detailed immunogenetic investigations are required in order to have a better prediction of the transplant outcome

Level of nitric oxide in bronchoalveolar lavage fluid of asthmatic mice model

Asthma is a chronic inflammatory disease with multifactorial and complicated mechanisms. Elevated level of exhaled Nitric Oxide [NO] in asthma and other inflammatory lung diseases has led to many studies examining NO as a potential marker of airway inflammation. This study was designed to determine the level of NO in Bronchoalveolar Lavage [BAL] fluid during early and late stages of asthmatic attack in mouse model. In this study male BALB/c mice were used. The level of NO was determined in BAL fluid of asthmatic mice five minutes, six and sixteen hours after challenge with methacholine, as irritant and smoke and 5% ovalbumin as allergens, using colorimetric assay. The level of NO increased upon exposure to all three irritants used in this study [52.3 microM for smoke and 49.5 [microMfor methacholine] as compared to 22.8 microM for the baseline. Our results showed that NO levels were increased during early phase of asthmatic condition and reached to its maximum level after six hours and decreased at the late stage of asthma [16hrs] possibly by activating a feedback regulatory loop. In addition, high level of NO led to the hypertrophy of smooth muscle that can account for the pathological changes associated with asthma. Thus, NO is an inflammatory marker in asthma and its measurement, as a non-invasive method during asthmatic attack is suggested. A careful development of specific inhibitors for iNOS enzyme during asthmatic attack is also necessary