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Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Rapid induction of autoantibodies during ARDS and septic shock | Burbelo et al. Journal of Translational Medicine 2010 8 97 http www.translational-medicine.eom content 8 1 97 JOURNAL OF TRANSLATIONAL MEDICINE RESEARCH Open Access Rapid induction of autoantibodies during ARDS and septic shock 1 2 3 1 1 1 4 Peter D Burbelo Nitin Seam Sandra Groot Kathryn H Ching Brian L Han G Umberto Meduri Michael J Iadarola 1 Anthony F Suffredini2 Abstract Background Little is known about the induction of humoral responses directed against human autoantigens during acute inflammation. We utilized a highly sensitive antibody profiling technology to study autoantibodies in patients with acute respiratory distress syndrome ARDS and severe sepsis conditions characterized by intensive immune activation leading to multiple organ dysfunction. Methods Using Luciferase Immunoprecipitation Systems LIPS a cohort of control ARDS and sepsis patients were tested for antibodies to a panel of autoantigens. Autoantibody titers greater than the mean plus 3 SD of the 24 control samples were used to identify seropositive samples. Available longitudinal samples from different seropositive ARDS and sepsis patient samples starting from within the first two days after admission to the intensive care were then analyzed for changes in autoantibody over time. Results From screening patient plasma 57 of ARDS and 46 of septic patients without ARDS demonstrated at least one statistically significant elevated autoantibody compared to the controls. Frequent high titer antibodies were detected against a spectrum of autoantigens including potassium channel regulator gastric ATPase glutamic decarboxylase-65 and several cytokines. Analysis of serial samples revealed that several seropositive patients had low autoantibodies at early time points that often rose precipitously and peaked between days 7-14. Further the use of therapeutic doses of corticosteroids did not diminish the rise in autoantibody titers. In some cases the patient autoantibody titers remained elevated through the
