Study of immunological biomarkers of saliva before and after cigarette smoke extract exposure to predict the risk of developing COPD

Aim. To study immunological biomarkers of saliva before and after cigarette smoke extract exposure to develop a model for predicting the likelihood of developing COPD. Material and methods. A survey of 84 respondents over 30 years of age was conducted. Among them, 41 patients had a verified diagnosis of COPD grade II-III (GOLD), the comparison group consisted of 43 practically healthy volunteers without obstructive airway pathology, 19 of whom (44,2%) had an allergological history (seasonal and year-round allergic rhinitis, conjunctivitis, drug allergy) and 24 (55,8%) healthy volunteers. Anamnestic, clinical, laboratory, and instrumental data of all examined patients was collected and analyzed. In the saliva samples obtained before and after cigarette smoke extract (CSE) exposure, the levels of IL-8, IL-13, NE, myeloperoxidase (MPO), lactoferrin, lysozyme, and leukotriene B4 were determined by enzyme immunoassay. Results. Differences in the levels of neutrophilic and T2 inflammation biomarkers in the saliva of patients with COPD compared to individuals without obstructive pulmonary diseases were established. In individuals with COPD, increased levels of lysozyme, lactoferrin, IL-13, and decreased levels of MPO were found in the saliva. Features of the immunological response after CSE exposure were found in patients with COPD. After CSE exposure in patients with COPD, an increased level of neutrophil elastase was detected among non-smokers compared to smokers, as well as between non-smoking patients with COPD and non-smokers from the control group. The level of IL-8 was also significantly higher in patients with COPD compared to healthy respondents without obstructive pathology. In addition, a significant increase in the level of MPO was found in the subgroup of non-smoking patients with COPD. Using multivariate regression analysis, the most significant factors associated with the probability of risk of developing COPD were established: smoking index, results of the COPD diagnostic questionnaire (CDQ)), FEV1, %, post-bronchodilator FEV1, %, FEV1/FVC, %, post-bronchodilator FEV1/FVC ratio, %, gender, the difference in IL-8 values before/after CSE exposure. Based on the data obtained, a mathematical model was developed that allows predicting risks of developing COPD in individuals without obstructive pulmonary pathology. Conclusions. A comprehensive method for predicting the risk of developing the neutrophilic inflammatory endotype COPD has been developed based on the use of available anamnestic, clinical diagnostic and immunological data, which will allow personalizing approaches to early diagnosis and prevention of COPD.