Currently, chronic obstructive pulmonary disease (COPD) is one of the leading causes of morbidity and mortality worldwide. The determination of immune mechanisms of inflammation in the disease presents an important challenge for fundamental medical research. According to modern views, Toll-like receptors (TLRs), among which TLR2 and TLR4 play a key role, are one of the essential components of inflammatory process in COPD. This review focuses on following aspects: the role of TLR2 and TLR4 in the initiation of inflammatory process in COPD; the mechanisms of influence of various exogenous factors (cigarette smoke, suspended particulate matter, and bacteria) on the expression of TLR2 and TLR4; the contribution of these TLRs to the T-helper (Th) immune response development in COPD, in particular to the Th17 immune response, which contributes to the progression of the disease and therapeutic implications of TLR2 and TLR4 in COPD.

ObjectiveTo study the mechanism of formation of air quality and to determine the impact of the studied factors on asthma morbidity in Vladivostok.MethodsThe evaluation of air pollution in Vladivostok was done using long-term (2008–2012) monitoring data (temperature, humidity, atmospheric pressure, wind speed, etc.). The levels of suspended particulate matter, nitrogen and sulfur dioxide, carbon monoxide, ammonia, formaldehyde (mg/m3) in six stationary observation posts were assessed. We studied the aerosol suspensions of solid particles, which were collected during snowfall from precipitation (snow) and air in 14 districts with different levels of anthropogenic impact. Melted snow was analyzed on laser granulometry. The impact of air pollution on the distribution of asthma morbidity was evaluated in various age groups by data of federal statistical observation obtained from 8 adults and 7 children municipal clinics in Vladivostok (2008–2012).ResultsThe content of suspended particulate components of pollution remained more stable, due to the features of atmospheric circulation, rugged terrain and residential development. The nano- and micro-sized particles (0–50 μm), which can absorb highly toxic metals, prevail in dust aerosols. These respirable fractions of particles, even in small doses, can contribute to the increase in asthma morbidity in the city.ConclusionsWe determined that asthma morbidity depends from general air pollution (in the range of 18.3%). It was detected that the highest age-specific dependence is associated with the content of particulate matter, carbon monoxide and nitrogen dioxide in air

Atmospheric microsized particles producing reactive oxygen species can pose a serious health risk for city residents. We studied the responses of organisms to microparticles in 255 healthy volunteers living in areas with different levels of microparticle air pollution. We analyzed the distribution of microparticles in snow samples by size and content. ELISA and flow cytometry methods were employed to determine the parameters of the thiol-disulfide metabolism, peroxidation and antioxidant, genotoxicity, and energy state of the leukocytes. We found that, in the park areas, microparticles with a size of 800 μm or more were predominant (96%), while in the industrial areas, they tended to be less than 50 μm (93%), including size 200–300 nm (7%). In the industrial areas, we determined the oxidative modification of proteins (21% compared to the park areas,p≤0.05) and DNA (12%,p≤0.05), as well as changes in leukocytes’ energy potential (53%,p≤0.05). An increase in total antioxidant activity (82%,p≤0.01) and thiol-disulfide system response (thioredoxin increasing by 33%,p≤0.01; glutathione, 30%,p≤0.01with stable reductases levels) maintains a balance of peroxidation-antioxidant processes, protecting cellular and subcellular structures from significant oxidative damage.

Background. Comorbidity of chronic obstructive pulmonary disease (COPD) and asthma (asthma COPD overlap syndrome, ACOS) is a significant problem in pulmonary practice, whose pathogenetic issues are not clarified yet.Objective. To study the features of the regulation of immune response in patients with comorbid COPD and asthma.Methods. We assessed the levels of CD3⁺, CD4⁺, CD8⁺, CD4⁺/CD8⁺, CD19⁺, CD25⁺, HLA-DR, total IgE, TNF-α, IL-4, IFN-γ, TXB₂, and LTB₄in patients with comorbid COPD and asthma.Results. The study involved 44 people with COPD, 39 people with asthma, and 12 people with comorbid COPD and asthma. The specific features in comorbid COPD and asthma were lymphocytosis, increased absolute count of T-helper cells, increased cytotoxic T-lymphocytes in relative and absolute count, increased relative and absolute numbers of B-lymphocytes, and high levels of total IgE. The elevated levels of TNF-αand IL-4 and inhibition of IFN-γproduction were detected. The content of LTB₄was maximal; TXB₂levels were higher than in control group but lower than in COPD and asthma.Conclusion. In comorbid COPD and asthma inflammation increased even during stable period. High levels of eicosanoids, low production of Th1-type cytokines, and active synthesis of opposition IL-4, along with increased IgE, indicate the activation of Th2-type immune response.