Abstract

Many studies have shown that the level of cell-free DNA (cfDNA) in blood of patients with oncological diseases, sepsis, systemic lupus erythematosus, and some rheumatic diseases significantly exceeds the value of similar index in healthy donors and is closely related to the clinical features of the disease. Systemic inflammatory response is among the most frequent pathophysiological processes along with markedly changed levels of cfDNA in blood plasma. The levels of cfDNA in blood plasma of patients with RA are shown to be closely associated with a shifted balance of helpers to the Th1-side. It is an adequate intensity index of inflammatory processes and effectiveness of therapy. At the same time, there only limited number of works concerning changes in cfDNA levels in pathological processes with predominance of Th2 lymphocytes. According to generally accepted concept, the pathogenesis of bronchial asthma is of distinct interest, being critically dependent on the production of specific antibodies controlled by activated Th2 lymphocytes. The aim of this work was to study the level of cfDNA in blood and compare its changes with intensity of NETs and inflammation in patients with asthma. The study included 20 patients with asthma, who underwent hospital treatment at the Department Allergology (Clinic of Immunopathology, RIFCI, Novosibirsk), and 10 conditionally healthy donors. We have shown that, upon admission to the clinic, the level of cfDNA in patients with asthma was significantly reduced against the control group of healthy donors. After a course of therapy, the average level of cfDNA in patients’ plasma was increased and did not differ statistically significantly from this index in controls. The data obtained for other parameters indicate that the patients with asthma did not reveal any signs of pronounced systemic inflammatory response. One should suggest that the observed changes in the level of cfDNA in blood plasma in bronchial asthma are not caused by chronic inflammatory process in lungs of these patients, but they are determined by some other pathophysiological mechanisms. It has been shown that the level of in vitro stimulated NETs in patients with asthma is higher than in healthy donors, thus being consistent with current opinions on the role of neutrophils in pathogenesis of asthma.

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