Abstract
Uncovering involvement of the purinergic system in the pathogenesis of ventilation disorders (VD) may provide additional information about the pathophysiological mechanisms leading to the development of VD in pulmonary tuberculosis (PT). The aim was to identify a relationship between the parameters of adenosine metabolism, inflammatory response and altered ventilation metabolism in PT patients. Materials and methods. Obstructive and mixed PT patients were assigned to subgroups with/without VD for assessing adenosine deaminase activity (ADA-1, 2) in serum, mononuclear cells, neutrophils; ecto-5’-nucleotidase (ecto-5’-NT); CD26 (dipeptidyl peptidase-4, DPP-4), phagocyte oxidative burst measured by NO generation. Results. PT patients showed decreased ADA-1 and CD26 (DPP-4), but increased ADA-2. Elevated intracellular adenosine concentration was found in mononuclear cells in patients lacking VD, whereas patients with mixed and obstructive VD — had it in neutrophils. Mononuclear cells of patients with PT lacking VD as well as with obstructive VD type had decreased NO3– concentration. Neutrophil hyperactivity was recorded in all groups of PT patients. Patients with PT lacking VD as well as with mixed VD type showed that the parameters of external respiration were associated with activity of extra-/intracellular ADA, whereas obstructive VD was caused by excessive formation of serum adenosine. Changes in respiratory function in PT were associated with decreased level of serum NO radicals, impaired nitrogen-dependent bactericidal phagocyte activity, and overproduced neutrophil oxygen radicals. Conclusion. Purinergic regulation is involved in regulating inflammatory and compensatory processes in PT patients as well as impaired ventilation efficiency. The most severe respiratory disorders observed in PT patients with mixed VD type are associated with the most prominent changes in nucleotidase activity, particularly ecto-ADA-2 and DPP-4/CD26.
Highlights
Аденозин образуется при расщеплении нуклеотидов активированными эктонуклеотидазами: внеклеточный АТФ/АДФ расщепляют эктонуклеозидтрифосфатдифосфогидролаза (NTPDases, CD39) и экто-5’-нуклеотидаза (CD73), а внутриклеточный, путем дефосфорилирования АМФ, — 5’-нуклеотидазы
Note. * — significant differences compared to reference group (RG)
Enzymatic and extraenzymatic role of adenosine deaminase 1 in T-celldendritic cell contacts and in alterations of the immune function
Summary
У больных ТЛ выявлены разнонаправленные изменения активности и концентрации ферментов в сыворотке крови (снижение АДА-1 и CD26 (ДПП-4) при повышении АДА-2). В мононуклеарах больных ТЛ без ВН и пациентов с обструктивным типом ВН регистрируется только снижение концентрации радикалов азота. У больных ТЛ без ВН и у больных со смешанным типом ВН параметры внешнего дыхания связаны с активностью вне-/ внутриклеточной АДА, тогда как обструктивные ВН обусловлены избыточным образованием аденозина в сыворотке крови, что обеспечивается концентрацией экто-5’-НТ и активностью АДА-2 в комплексе с CD26 (ДПП-4). Изменения функции внешнего дыхания у больных ТЛ связаны со снижением концентрации радикалов оксида азота в сыворотке крови, нарушением азот-зависимой бактерицидности фагоцитов, гиперпродукцией кислородных радикалов активированными нейтрофилами. Для цитирования: Дьякова М.Е., Серебряная Н.Б., Кирюхина Л.Д., Эсмедляева Д.С., Яблонский П.К.
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