Mechanisms Of Lung Damage Research Articles

Mechanisms of lung damage in tuberculosis: implications for chronic obstructive pulmonary disease.

Pulmonary tuberculosis is increasingly recognized as a risk factor for COPD. Severe lung function impairment has been reported in post-TB patients. Despite increasing evidence to support the association between TB and COPD, only a few studies describe the immunological basis of COPD among TB patients following successful treatment completion. In this review, we draw on well-elaborated Mycobacterium tuberculosis-induced immune mechanisms in the lungs to highlight shared mechanisms for COPD pathogenesis in the setting of tuberculosis disease. We further examine how such mechanisms could be exploited to guide COPD therapeutics.

Mechanisms of Lung Damage and Development of COPD Due to Household Biomass-Smoke Exposure: Inflammation, Oxidative Stress, MicroRNAs, and Gene Polymorphisms

Chronic exposure to indoor biomass smoke from the combustion of solid organic fuels is a major cause of disease burden worldwide. Almost 3 billion people use solid fuels such as wood, charcoal, and crop residues for indoor cooking and heating, accounting for approximately 50% of all households and 90% of rural households globally. Biomass smoke contains many hazardous pollutants, resulting in household air pollution (HAP) exposure that often exceeds international standards. Long-term biomass-smoke exposure is associated with Chronic Obstructive Pulmonary Disease (COPD) in adults, a leading cause of morbidity and mortality worldwide, chronic bronchitis, and other lung conditions. Biomass smoke-associated COPD differs from the best-known cigarette smoke-induced COPD in several aspects, such as a slower decline in lung function, greater airway involvement, and less emphysema, which suggests a different phenotype and pathophysiology. Despite the high burden of biomass-associated COPD, the molecular, genetic, and epigenetic mechanisms underlying its pathogenesis are poorly understood. This review describes the pathogenic mechanisms potentially involved in lung damage, the development of COPD associated with wood-derived smoke exposure, and the influence of genetic and epigenetic factors on the development of this disease.

Pneumosclerotic changes in lung tissues as a sign of tumor transformation in workers of the main professions of coal mines

Introduction. The workers of coal mines are characterized by a high level of not only occupational diseases, but also oncological diseases. Modern knowledge in the field of studying pneumoconiosis contains many contradictions in the assessment of the pathogenetic mechanisms of lung damage, in particular, the morphogenesis of neoplastic changes in the respiratory system at the final stage of the disease with pronounced sclerotic changes. The study is devoted to the occurrence and development of tumor tissue in the miners working in the underground conditions. The task is to identify morphological trigger mechanisms for the development of oncological pathology in miners, relying on pathomorphological, immunohistochemical studies of the changes in the epithelial tissue of the airways, as well as various cellular communities of the bronchi, blood vessels of the lungs and lung tissue parenchyma using the example of epithelial-mesenchymal transformation under dust load. The purpose of this study was to determine the influence of the fibroplastic process on the development of oncological pathology in miners who worked in underground conditions. Materials and methods. Histological, immunohistochemical and morphometric studies of the respiratory system obtained during 50 autopsy works of a group of Kuzbass miners working in underground conditions was carried out. Cancer of various localization and histogenetic affiliation was previously diagnosed in 20 miners. The mucous membrane of the bronchi, respiratory tissue of the lungs, arteries and veins of the pulmonary circulation were studied. Immunohistochemical study was performed using monoclonal antibodies (marker of proliferation Ki-67, oncogene of proapoptotic activity Bcl-2, growth and neoangiogenesis factors, endothelial function factors CD-31 and CD-34, marker of epithelial tissue cytokeratin (cyt), muscle tissue markers - actin, desmin, vimentin, connective tissue markers - collagen, laminil, markers of intercellular interactions EMA, SMA). Results. Transformed fibroblasts, myofibroblasts are a cell population of dedifferentiated epithelial tissue with different expressions of nonspecific markers (desmin, actin, vimentin), capable of tumor transformation. Sclerotic tissue changes in pneumoconiosis are the areas of tumor transdifferentiation. Fibroblasts with an altered phenotype, namely myofibroblasts, are able to give rise to the growth of undifferentiated mesenchymal cell communities (tumor tissue), including atypical epithelial cells, adipocytes, chondrocytes and endotheliocytes. Conclusions. Epithelial-mesenchymal transformation can be a triggering mechanism for the development of tumor transformation from extensive fibrosed zones in miners with dust lung pathology. In this case, the main etiological factor of tumor progression is activated fibroplastic cells.

COVID-19 lung damage: Diagnostics and treatment at the primary health care

The lecture is devoted to lung damage in new coronavirus infection. The description of the pathogenetic mechanisms of lung damage is given. The characteristics of the morphological changes in the lungs with severe disease and their characteristics are given. Provides information on instrumental and laboratory diagnosis of lung lesions in COVID-19. Particular attention is paid to highlighting controversial and complex issues of managing patients with lung damage in COVID-19 in outpatient practice. In particular, controversial issues of terminology for defining lung damage, the complexity of differentiating viral lung damage and other causes, the complexity of diagnosing bacterial superinfection and its treatment. Aspects of patient management important for primary care physician are highlighted: current treatment regimens for COVID-19 patients with lung damage, the timing of the control X-ray examination. It provides information on the most common mistakes encountered in the management of patients with COVID-19 (over-prescribing radiation methods, over-prescribing antibacterial medications).

Role of oxidative stress in preterm infants with bronchopulmonary dysplasia after exposure to chorioamnionitis

Inflammation is one of the main causes of preterm birth, frequently associated to intrauterine infection or chorioamnionitis. Oxidative stress is involved in preterm birth. On the one hand, reactive oxygen species are released by inflammatory cells against infection; on the other hand it is responsible of placental tissue damage after chorioamnionitis. Because of improvement in obstetric and perinatal care, survival rate in preterm births has increased, leading to changes in pathology of several processes, such as bronchopulmonary dysplasia. Bronchopulmonary dysplasia is a multifactorial entity which is consequence of multiple mechanisms, including perinatal inflammation and oxygen free radicals. Preterm newborn is very susceptible to chronic lung damage because of both, low antioxidant capacity, and exposure to high oxygen fractions during postnatal life. Modest lung oxidative stress damage after exposure to fetal endotoxin in premature newborns has been shown. Postnatal injury is needed to amplify the intrauterine inflammatory damage. Cell death induction by reactive oxygen species has been suggested as mechanism of lung damage. Several antioxidant therapies have been used in experimental studies in order to reduce or prevent bronchopulmonary dysplasia. So far, care is needed to standardize its use, because of its undesirable effects on inflammatory defense and development.

Intrahepatic Cholestasis of Pregnancy and Bile Acids Induced Lung Injury in Newborn Infants

Intrahepatic cholestasis of pregnancy (ICP) is a clinical syndrome of unknown pathophysiology, occurring during the second half of pregnancy and persisting until delivery. The incidence of ICP varies from 0.1% to 1.5% of pregnancies in Europe, North America and Australia and from 9.2% to 15.6% in South American countries such as Bolivia and Chile. This syndrome has been associated with increased foetal distress, intrauterine death, premature delivery, perinatal mortality and, more recently, with the occurrence of respiratory distress syndrome in the newborn infant. Bile acids (BA) are supposed to be the main mediators for these complications because ICP seriously impairs the placental clearance of foetal BA leading to a dangerous accumulation of these compounds within the foetus and the newborn. Cholestatic pregnancies have to be considered high risk ones, recent reports showing that BA can interfere with surfactant metabolism and are particularly harmful for the developing lung. This review summarizes existing literature data on this topic with particular emphasis on bile acids-induced lung injury. The authors discuss possible mechanisms of lung damage and highlight future research perspectives in this field.

Alveolar overdistension is an important mechanism of persistent lung damage following severe protracted ARDS.

It is now widely accepted that mechanical ventilation may damage the lung, but the mechanism of lung damage is not clear. Possible causes include overdistension of aerated alveoli by inappropriately large tidal volumes (volutrauma), shear stresses generated during the recruitment and de-recruitment of lung units at the junction of aerated and collapsed lung, and infective or ischaemic necrosis of persistently collapsed lung. Computerized tomography allows noninvasive assessment of lung structure during and after acute lung injury, and may provide insight into the mechanism of lung damage. Using serial high resolution computed tomography we documented lung structure one month after recovery from severe protracted adult respiratory distress syndrome (ARDS) in three patients who required mechanical ventilation for between 86 and 97 days; the computed tomograms were repeated at between 5 and 14 months. All three patients had persistent abnormalities of lung structure which were most marked in the anterior regions of the lung. These findings suggest that overdistension of non-dependent lung regions in the main mechanism of lung damage persisting after recovery from severe protracted ARDS.