Emerging Insights into the Impact of Air Pollution on Immune-Mediated Asthma Pathogenesis.

PURPOSE OF REVIEW: Increases in ambient levels of air pollutants have been linked to lung inflammation and remodeling, processes that lead to the development and exacerbation of allergic asthma. Conventional research has focused on the role of CD4+ T helper 2 (TH2) cells in the pathogenesis of air pollution-induced asthma. However, much work in the past decade has uncovered an array of air pollution-induced non-TH2 immune mechanisms that contribute to allergic airway inflammation and disease. RECENT FINDINGS: In this article, we review current research demonstrating the connection between common air pollutants and their downstream effects on non-TH2 immune responses emerging as key players in asthma, including PRRs, ILCs, and non-TH2 T cell subsets. We also discuss the proposed mechanisms by which air pollution increases immune-mediated asthma risk, including pre-existing genetic risk, epigenetic alterations in immune cells, and perturbation of the composition and function of the lung and gut microbiomes. Together, these studies reveal the multifaceted impacts of various air pollutants on innate and adaptive immune functions via genetic, epigenetic, and microbiome-based mechanisms that facilitate the induction and worsening of asthma.

Fibroin-Gelatin Composite Stimulates the Regeneration of a Splinted Full-Thickness Skin Wound in Mice.

The effects of composite fibroin-gelatin microparticles (100-250 µ) on the rate of wound healing and regeneration under conditions of contraction prevention were studied on the model of splinted full-thickness skin wound in a mouse. Subcutaneous injection of these particles into the defect area accelerated wound healing and promoted re-epithelialization and recovery of normal structure of the epidermis. In addition, the composite microparticles promoted the formation of connective tissue of characteristic structure, replacing the derma over the entire defect, and stimulated regeneration of subcutaneous muscle (panniculus carnosus) and skin appendages (sebaceous glands and hair follicles).

Effect of unilateral diaphragmatic paralysis on postpneumonectomy lung growth.

Respiratory muscle-associated stretch has been implicated in normal lung development (fetal breathing movements) and postpneumonectomy lung growth. To test the hypothesis that mechanical stretch from diaphragmatic contraction contributes to lung growth, we performed left phrenic nerve transections (PNT) in mice with and without ipsilateral pneumonectomy. PNT was demonstrated by asymmetric costal margin excursion and confirmed at autopsy. In mice with two lungs, PNT was associated with a decrease in ipsilateral lung volume (P<0.05) and lung weight (P<0.05). After pneumonectomy, PNT was not associated with a change in activity level, measureable hypoxemia, or altered minute ventilation; however, microCT scanning demonstrated altered displacement and underinflation of the cardiac lobe within the first week after pneumonectomy. Coincident with the altered structural realignment, lung impedance measurements, fitted to the constant-phase model, demonstrated elevated airway resistance (P<0.05), but normal peripheral tissue resistance (P>0.05). Most important, PNT appeared to abrogate compensatory lung growth after pneumonectomy; the weight of the lobes of the right lung was significantly less than pneumonectomy alone (P<0.001) and indistinguishable from nonsurgical controls (P>0.05). We conclude that the cyclic stretch associated with diaphragmatic muscle contraction is a controlling factor in postpneumonectomy compensatory lung growth.

[Quality of life and characteristics of the external respiration function in patients with bronchial asthma]. / Kachestvo zhizni i pokazateli funktsii vneshnego dykhaniia u bol'nykh s bronkhial'noi astmoi.

AIM: To investigate correlations between quality of life, bronchial obstruction, nonspecific bronchial hyperreactivity (NSBH) and response of these parameters to treatment with inhalation steroids in patients with bronchial asthma (BA). MATERIAL AND METHODS: The study included 67 BA patients (47 women and 20 men) aged 18 to 62 years (mean age 43 years). 59 of them had the diagnosis of atopic BA, 8 had bacterial BA. Quality of life was assessed with the questionnaire AQLQ, bronchial obstruction was judged by forced expiratory volume per a second (FEV1). Bronchial hyperreactivity was studied with acetylcholine and histamine tests. RESULTS: Quality of life strongly correlated with FEV1 and NSBH. Positive changes in the latter due to treatment with inhalation glucocorticoid budesonide (400 mcg/day) entailed improvement of life quality. CONCLUSION: Bronchial obstruction and NSBH have a significant effect on BA patients' life quality which should be considered in monitoring of BA patients' condition.

[Hydrogen peroxide--a marker for respiratory tract inflammation in patients with bronchial asthma]. / Perekis' vodoroda kak marker vospaleniia dykhatel'nykh putei u bol'nykh bronkhial'noi astmoi.

AIM: To test H2O2 as a marker of respiratory tract inflammation in patients with bronchial asthma (BA). MATERIAL AND METHODS: The study entered 70 patients (20 males and 50 females) with atopic asthma (AA) aged 18 to 62 years (mean age 32.6 years). H2O2 concentration in the expired air (CEA) was determined spectrophotometrically (Gallati & Pracht, 1985), content of eosinophilic cationic protein (ECP) in blood--with radioimmunoassay kits (Pharmacia & Upjohn, Sweden). Forced expiratory volume per 1 second (FEV1) was used for assessment of severity of bronchial obstruction. Bronchial hyperreactivity was studied by means of the histamine bronchoprovocative test. RESULTS: H2O2 in CEA in BA patients was higher than in healthy subjects (0.127 +/- 0.010 microm/l vs 0.024 +/- 0.004 microm/l). H2O2 concentration significantly correlates with FEV1 (r = -0.449; p < 0.001), bronchial hyperreactivity to histamine (rs = -0.382; p < 0.05) and ECP in blood plasma(r = 0.625; p < 0.01). CONCLUSION: It was proved possible to use H2O2 in CEA for evaluation of respiratory inflammation in BA patients.