Adenosine-regulated mechanisms in the pathogenesis of ventilation disorders in patients with pulmonary tuberculosis

Abstract

Disclosure of the purinergic system involvement in the ventilation disorders (VD) pathogenesis can provide additional information about the pathophysiological mechanisms leading to the VD development in pulmonary tuberculosis (PT) patients.

The aim: to study the relationship of adenosine metabolism parameters with ventilation and gas exchange disorders in PT patients.

Methods: PT patients without VD (n=23, 1 gr), obstructive (n=26, 2 gr) and mixed (n=11, 3gr) types of VD were studied adenosine deaminase activity (ADA-1, 2) in serum (s), in mononuclear cells (mn), in neutrophils (nph); 5'-nucleotidase (5'-NT) in s; CD26 (dipeptidyl peptidase-4, DPP-4) in s, mn.

Results: Patients of all groups showed an increase in ADA-2s (Me>12.0 U/l), 5'-NTs (>0.75 ng/ml) and a decrease in CD26 (DPP-4) mn (<3.8 ng/ml; p<0.05 for all). Decrease in ADA-1s (<2.3 U/l) - in 1 gr and 2 gr, ADA-1mn (1.03 U/106 cells) - in 1 gr, ADA-1nph (<1.2 U/106 cells) - in 2 and 3 gr (p<0.05 of all). The activity of ADA-2s in patients of the 3rd group was higher (19.0 U/l) than in 1 (14.8 U/l) and 2 (12.0 U/l; p<0.05). In 1 and 3gr. VD was associated with ADA-2s and ADA-1nph, whereas in 2 gr – with 5'-NT and CD26 (DPP-4).

Conclusion: Purinergic regulation is involved in the regulation of inflammatory and compensatory processes in pulmonary tuberculosis patients. It is associated with the clinical course of the disease, including impaired ventilation efficiency. The most severe respiratory disorders observed in the group of PT patients with mixed type of VD were associated with the most pronounced changes in the nucleotidase enzymes activity, in particular ecto-ADA-2 and CD26 (DPP-4).