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International Journal of Molecular... Apr 2020Gas exchange in the lung takes place via the air-blood barrier in the septal walls of alveoli. The tissue elements that oxygen molecules have to cross are the alveolar... (Review)
Review
Gas exchange in the lung takes place via the air-blood barrier in the septal walls of alveoli. The tissue elements that oxygen molecules have to cross are the alveolar epithelium, the interstitium and the capillary endothelium. The epithelium that lines the alveolar surface is covered by a thin and continuous liquid lining layer. Pulmonary surfactant acts at this air-liquid interface. By virtue of its biophysical and immunomodulatory functions, surfactant keeps alveoli open, dry and clean. What needs to be added to this picture is the glycocalyx of the alveolar epithelium. Here, we briefly review what is known about this glycocalyx and how it can be visualized using electron microscopy. The application of colloidal thorium dioxide as a staining agent reveals differences in the staining pattern between type I and type II alveolar epithelial cells and shows close associations of the glycocalyx with intraalveolar surfactant subtypes such as tubular myelin. These morphological findings indicate that specific spatial interactions between components of the surfactant system and those of the alveolar epithelial glycocalyx exist which may contribute to the maintenance of alveolar homeostasis, in particular to alveolar micromechanics, to the functional integrity of the air-blood barrier, to the regulation of the thickness and viscosity of the alveolar lining layer, and to the defence against inhaled pathogens. Exploring the alveolar epithelial glycocalyx in conjunction with the surfactant system opens novel physiological perspectives of potential clinical relevance for future research.
Topics: Alveolar Epithelial Cells; Animals; Glycocalyx; Humans; Pulmonary Alveoli; Pulmonary Surfactants; Respiratory Mucosa
PubMed: 32349261
DOI: 10.3390/ijms21093075 -
International Journal of Molecular... Oct 2022Asthma is a chronic inflammatory airway disease characterized by variable airflow obstruction, bronchial hyper-responsiveness, and airway inflammation. The chronic... (Review)
Review
Asthma is a chronic inflammatory airway disease characterized by variable airflow obstruction, bronchial hyper-responsiveness, and airway inflammation. The chronic inflammation of the airway is mediated by many cell types, cytokines, chemokines, and inflammatory mediators. Research suggests that exposure to air pollution has a negative impact on asthma outcomes in adult and pediatric populations. Air pollution is one of the greatest environmental risks to health, and it impacts the lungs' innate and adaptive defense systems. A major pollutant in the air is particulate matter (PM), a complex component composed of elemental carbon and heavy metals. According to the WHO, 99% of people live in air pollution where air quality levels are lower than the WHO air quality guidelines. This suggests that the effect of air pollution exposure on asthma is a crucial health issue worldwide. Macrophages are essential in recognizing and processing any inhaled foreign material, such as PM. Alveolar macrophages are one of the predominant cell types that process and remove inhaled PM by secreting proinflammatory mediators from the lung. This review focuses on macrophages and their role in orchestrating the inflammatory responses induced by exposure to air pollutants in asthma.
Topics: Humans; Adult; Child; Air Pollution; Air Pollutants; Asthma; Particulate Matter; Macrophages, Alveolar; Inflammation; Cytokines; Inflammation Mediators; Carbon; Environmental Exposure
PubMed: 36293195
DOI: 10.3390/ijms232012337 -
Annals of Work Exposures and Health Oct 2019Increased rates of leukaemia have been found among tanker crews. Occupational exposures to the leukomogen benzene during loading, unloading, and tank cleaning are...
INTRODUCTION
Increased rates of leukaemia have been found among tanker crews. Occupational exposures to the leukomogen benzene during loading, unloading, and tank cleaning are possible causes. Studies on older types of tankers carrying gasoline with most handling being done manually have revealed important exposures to benzene. Our study explores benzene exposures on tankers with both automatic and manual systems. Correlations between benzene exposure and benzene in alveolar air (AlvBe), benzene in urine (UBe), and trans,trans-muconic acid (ttMA) in urine were investigated.
METHODS
Forty-three male seafarers (22 deck crewmembers and 21 not on deck) on five Swedish different product and chemical tankers transporting 95- or 98-octane gasoline were investigated between 1995 and 1998. The tankers used closed systems for the loading and unloading of gasoline but stripping and tank cleaning were done manually. Benzene in respiratory air was measured using personal passive dosimeters during a 4-h work shift. Samples for biomarker analyses were collected pre- and post-shift. Smoking did occur and crewmembers did not use any respiratory protection during work.
RESULTS
The average 4-h benzene exposure level for exposed was 0.45 mg m-3 and for non-exposed 0.02 mg m-3. Benzene exposure varied with type of work (range 0.02-143 mg m-3). AlvBe, UBe, and ttMA were significantly higher in post-shift samples among exposed and correlated with exposure level (r = 0.89, 0.74, and 0.57, respectively). Smoking did not change the level of significance among exposed.
DISCUSSION
Benzene in alveolar air, unmetabolized benzene, and ttMA in urine are potential biomarkers for occupational benzene exposure. Biomarkers were detectable in non-exposed, suggesting benzene exposure even for other work categories on board tankers. Work on tankers carrying gasoline with more or less closed handling of the cargo may still lead to significant benzene exposure for deck crewmembers, and even exceed the Swedish Occupational Exposure Limit (OEL; 8-h time-weighted average [TWA]) of 1.5 mg m-3.
Topics: Adult; Air Pollutants, Occupational; Benzene; Biomarkers; Environmental Monitoring; Gasoline; Humans; Male; Middle Aged; Occupational Exposure; Pulmonary Alveoli; Sorbic Acid; Young Adult
PubMed: 31382272
DOI: 10.1093/annweh/wxz055 -
The European Respiratory Journal May 2016Mechanisms for the adverse respiratory effects of traffic-related air pollution (TRAP) have yet to be established. We evaluated the acute effects of TRAP exposure on...
Mechanisms for the adverse respiratory effects of traffic-related air pollution (TRAP) have yet to be established. We evaluated the acute effects of TRAP exposure on proximal and distal airway inflammation by relating indoor nitric oxide (NO), a marker of TRAP exposure in the indoor microenvironment, to airway and alveolar sources of exhaled nitric oxide (FeNO).FeNO was collected online at four flow rates in 1635 schoolchildren (aged 12-15 years) in southern California (USA) breathing NO-free air. Indoor NO was sampled hourly and linearly interpolated to the time of the FeNO test. Estimated parameters quantifying airway wall diffusivity (DawNO) and flux (J'awNO) and alveolar concentration (CANO) sources of FeNO were related to exposure using linear regression to adjust for potential confounders.We found that TRAP exposure indoors was associated with elevated alveolar NO. A 10 ppb higher indoor NO concentration at the time of the FeNO test was associated with 0.10 ppb higher average CANO (95% CI 0.04-0.16) (equivalent to a 7.1% increase from the mean), 4.0% higher J'awNO (95% CI -2.8-11.3) and 0.2% lower DawNO (95% CI -4.8-4.6).These findings are consistent with an airway response to TRAP exposure that was most marked in the distal airways.
Topics: Adolescent; Air Pollution, Indoor; Asthma; Automobiles; Breath Tests; California; Child; Cohort Studies; Cross-Sectional Studies; Environmental Exposure; Exhalation; Female; Humans; Inflammation; Linear Models; Luminescence; Male; Nitric Oxide; Pulmonary Alveoli; Spirometry
PubMed: 26797034
DOI: 10.1183/13993003.01176-2015 -
Neonatology 2017In human neonates rapid adaptation from an aqueous intrauterine environment to permanent air breathing is the rate-limiting step for extrauterine life, failure of which... (Review)
Review
In human neonates rapid adaptation from an aqueous intrauterine environment to permanent air breathing is the rate-limiting step for extrauterine life, failure of which justifies the existence of neonatal intensive care units. The lung develops at about 4-6 weeks' gestation in humans as a ventral outpouching of the primitive foregut into the surrounding ventral mesenchyme, termed the laryngotracheal groove. At its posterior end lie progenitor cells that form a pair of bronchial tubes, from which arise all the distal epithelial structures of the lung. In humans, formation of the distal gas exchange surfaces begins in utero at about 20 weeks' gestation and is substantially established by term. Stereotypic branching of the proximal airway ends relatively early at 16-18 weeks at the bronchoalveolar duct junctions. Distally, about 5 finger-like alveolar ducts arise from each bronchoalveolar duct junction and ramify outwards towards the pleura. The majority of alveolar air sacs arise from the sides of the alveolar ducts and each of these alveoli can have up to 5 daughter alveoli arising from the outer surface as subsequent buds. At the end of each alveolar duct lie the mouths of 5 interconnected alveoli. Each family of alveoli arising from each bronchoalveolar duct junction has a different shape depending upon the limitations imposed by the pleural surface as well as the interstitial fascial planes.
Topics: Animals; Fetal Development; Gestational Age; Humans; Infant, Newborn; Lung
PubMed: 28538234
DOI: 10.1159/000458465 -
Revue Medicale de Liege Mar 2021Presence of air in the spinal canal, called pneumorrhachis (PR) is a rare and likely unrecognized condition often due to traumatic or iatrogenic causes. Most of PR occur...
Presence of air in the spinal canal, called pneumorrhachis (PR) is a rare and likely unrecognized condition often due to traumatic or iatrogenic causes. Most of PR occur after repeated epidural ponction or penetrating trauma or brutal intra-alveolar increase especially in asthma attack. Non traumatic and non iatrogenic causes are uncommon but can appear in a neoplastic context.
Topics: Asthma; Humans; Pneumorrhachis; Spinal Canal
PubMed: 33682380
DOI: No ID Found -
American Journal of Physiology. Lung... Dec 2004This essay looks at the historical significance of four APS classic papers that are freely available online: Fenn WO, Rahn H, and OTIS AB. A theoretical study of the...
This essay looks at the historical significance of four APS classic papers that are freely available online: Fenn WO, Rahn H, and OTIS AB. A theoretical study of the composition of the alveolar air at altitude. Am J Physiol 146: 637-653. 1946 (http://ajplegacy.physiology.org/cgi/reprint/146/5/637). Rahn H. A concept of mean alveolar air and the ventilation-bloodflow relationships during pulmonary gas exchange. Am J Physiol 158: 21-30, 1949 (http://ajplegacy.physiology.org/cgi/reprint/158/1/21)). Riley RL. And Cournand A. "Ideal" Alveolar air and the analysis of ventilation-perfusion relationships in the lungs. J Appl Physiol 1: 825-847. 1949 (http://jap.physiology.org/cgi/reprint/1/12/825). Riley RL. And Cournand A. Analysis of factors affecting partial pressures of oxygen and carbon dioxide in gas and blood of lungs: theory. J Appl Physiol 4: 77-101. 1951 (http://jap.physiology.org/cgi/reprint/4/2/77).
Topics: Humans; Lung; Models, Biological; Pulmonary Gas Exchange
PubMed: 15531755
DOI: 10.1152/classicessays.00024.2004 -
Stem Cell Research & Therapy Jul 2023Acute lung injury is characterized by overwhelmingly elevated PAI-1 in both lung edema fluid and the circulating system. The role of increased PAI-1, encoded by Serpine1...
BACKGROUND
Acute lung injury is characterized by overwhelmingly elevated PAI-1 in both lung edema fluid and the circulating system. The role of increased PAI-1, encoded by Serpine1 gene, in the regeneration of injured lung epithelium has not been understood completely. This study aimed to investigate the role of Serpine1 in the regulation of alveolar type 2 epithelial cell (AT2) fate in a humanized mouse line carrying diseased mutants (Serpine1).
METHODS
Wild-type (wt) and Serpine1 AT2 cells were either cultured as monolayers or 3D alveolospheres. Colony-forming assay and total surface area of organoids were analyzed. AT1 and AT2 cells in organoids were counted by immunohistochemistry and fluorescence-activated cell sorting (FACS). To test the potential effects of elevated PAI-1 on the permeability in the epithelial monolayers, we digitized the biophysical properties of polarized AT2 monolayers grown at the air-liquid interface.
RESULTS
A significant reduction in total AT2 cells harvested in Serpine1 mice was observed compared with wt controls. AT2 cells harvested from Serpine1 mice reduced significantly over the wt controls. Spheroids formed by Serpine1 AT2 cells were lesser than wt control. Similarly, the corresponding surface area, a readout of re-alveolarization of injured epithelium, was markedly reduced in Serpine1 organoids. FACS analysis revealed a significant suppression in the number of AT2 cells, in particular, the CD44 subpopulation, in Serpine1 organoids. A lesser ratio of AT1:AT2 cells in Serpine1 organoids was observed compared with wt cultures. There was a significant increase in transepithelial resistance but not amiloride inhibition.
CONCLUSIONS
Our study suggests elevated PAI-1 in injured lungs downregulates alveolar epithelial regeneration by reducing the AT2 self-renewal, particularly in the CD44 cells.
Topics: Mice; Animals; Plasminogen Activator Inhibitor 1; Cells, Cultured; Alveolar Epithelial Cells; Lung; Permeability
PubMed: 37501095
DOI: 10.1186/s13287-023-03414-4 -
Progress in Cardiovascular Diseases 2015Cardiac dysfunction of both systolic and diastolic origins leads to increased left atrial pressure, lung capillary injury and increased resistance to gas transfer.... (Review)
Review
Cardiac dysfunction of both systolic and diastolic origins leads to increased left atrial pressure, lung capillary injury and increased resistance to gas transfer. Acutely, pressure-induced trauma disrupts the endothelial and alveolar anatomical configuration and definitively causes an impairment of cellular pathways involved in fluid-flux regulation and gas exchange efficiency, a process well identified as stress failure of the alveolar-capillary membrane. In chronic heart failure (HF), additional stimuli other than pressure may trigger the true remodeling process of capillaries and small arteries characterized by endothelial dysfunction, proliferation of myofibroblasts, fibrosis and extracellular matrix deposition. In parallel there is a loss of alveolar gas diffusion properties due to the increased path from air to blood (thickening of extracellular matrix) and loss of fine molecular mechanism involved in fluid reabsorption and clearance. Deleterious changes in gas transfer not only reflect the underlying lung tissue damage but also portend independent prognostic information and may play a role in the pathogenesis of exercise limitation and ventilatory abnormalities observed in these patients. Few currently approved treatments for chronic HF have the potential to positively affect structural remodeling of the lung capillary network; angiotensin-converting enzyme inhibitors are one of the few currently established options. Recently, more attention has been paid to novel therapies specifically targeting the nitric oxide pathway as a suitable target to improve endothelial function and permeability as well as alveolar gas exchange properties.
Topics: Animals; Blood-Air Barrier; Capillaries; Capillary Permeability; Endothelium, Vascular; Heart Failure; Humans; Hypertension, Pulmonary; Lung; Lung Diseases; Prognosis; Pulmonary Gas Exchange; Risk Factors; Vascular Remodeling
PubMed: 25446556
DOI: 10.1016/j.pcad.2014.11.003