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The respiratory system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The disease is initiated by damage to the pulmonary endothelium or the epithelium leading to endothelial activation and neutrophil adhesion. The early changes vary depending on which side of the basement membrane the insult occurs. Early signs of pneumocyte injury include separation from the basement membrane. There is also type II pneumocyte damage, affecting surfactant production. Endothelial cell damage is characterized by endothelial cell swelling and development of interstitial oedema. With loss of type I cells, fibrin leaks through epithelial cell junctions. The mixture of fibrin, dead cells, and plasma proteins makes up hyaline membranes (Figure 8.9). Early alveolar wall congestion progresses to give rise to fibrin thrombi in arteries and capillaries (disseminated intravascular coagulation) and an increase in megakaryocytes in the pulmonary capillaries releasing platelets. The release of inflammatory cytokines stimulates fibroblast ingrowth to repair the gap left by the damaged type I cells. As early as 48 hours, loose myxoid interstitial and sometimes intra-alveolar fibrosis (organizing pneumonia pattern) begin. The hyaline membranes and organizing pneumonia result in impaired gas exchange and respiratory failure.
Human Coronavirus Respiratory Infections
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
Thomas Edward Cecere, Stephanie Michelle Todd, Owen Benjamin Richmond
Patients that succumbed during early SARS had diffuse alveolar damage that included hyaline membrane formation, edema, vascular thrombosis, fibrinous exudate, pneumocyte loss and sloughing, and mixed inflammation consisting of lymphocytes, macrophages, and neutrophils. Those that died following chronic infection exhibited lung lesions that included type II pneumocyte hyperplasia, squamous metaplasia, syncytial cell formation, and bronchiolitis obliterans (Figure 27.4).7
Developmental Aspects of the Alveolar Epithelium and the Pulmonary Surfactant System
Published in Jacques R. Bourbon, Pulmonary Surfactant: Biochemical, Functional, Regulatory, and Clinical Concepts, 2019
Jacques R. Bourbon, Caroline Fraslon
Between 22 and 24 weeks, the acinar channels take a wavy internal configuration,16 announcing their subsequent subdivision. It is during this period that the first morphologically differentiated type II pneumocytes, i.e., epithelial cells containing lamellar bodies, were described classically.8 More recent investigation with the transmission electron microscope has, however, revealed the emergence of typical lamellar bodies on the 19th week.18 Furthermore, the approach, consisting of using antibodies to identify antigenic molecules unique for this cell type — an approach recently designated “immunotargeting”19 — allowed identification of type II cells or their precursors as early as 10 to 12 weeks20 and at corresponding precocious stages in rodents.21–23 For instance, an antigen expressed by rat alveolar type II cells (a glycoprotein of approximate molecular weight 146,000), but not type I cells or other mature lung cells, was already expressed by cuboidal epithelial cells lining the respiratory ducts of the first divisions of the tracheal bud, but not tracheal cells themselves.23 It was expressed by epithelial cells of the larger respiratory ducts until 19 weeks of gestation, i.e., around the times of appearance of lamellar bodies.23 Thereafter, its expression was limited to cells of the smallest ducts and finally to fully differentiated type II cells.23 These data suggest that the type II pneumocyte is probably committed during the early pseudoglandular stage and could presumably represent the basic cell type of pulmonary epithelium.
Alteration of the gut microbiota’s composition and metabolic output correlates with COVID-19-like severity in obese NASH hamsters
Published in Gut Microbes, 2022
Valentin Sencio, Nicolas Benech, Cyril Robil, Lucie Deruyter, Séverine Heumel, Arnaud Machelart, Thierry Sulpice, Antonin Lamazière, Corinne Grangette, François Briand, Harry Sokol, François Trottein
Compared with hamsters fed a standard chow, hamsters fed a free-choice high fat/high cholesterol diet with drinking water enriched with 10% fructose for 20 weeks displayed higher body weight, suffered from dyslipidemia (e.g. higher serum levels of total cholesterol and triglycerides), and developed a substantial NASH and liver fibrosis phenotype (Figure 1a). We then investigated the effects of SARS-CoV-2 infection in lean hamsters and in free choice diet-induced obese NASH hamsters. Both groups showed a substantial reduction in body weight on post-infection day 7 (D7) (Supplementary Figure S1a) but started to recover thereafter (sacrifice at D10). With regard to lung disease, lean hamsters and obese NASH hamsters developed similar bronchointerstitial pneumonia at D4, together with bronchiolar epithelial cell death/necrosis, alveolar septal congestion, edema, and patchy alveolar hemorrhage (Supplementary Figure S1b). Lung inflammation was still severe at D10, and type II pneumocyte hyperplasia was clearly evidenced. Interestingly, lung lesions at D10 were more severe in obese NASH hamsters than in lean hamsters (Figure 1b and 1c).
Could Vitamin C Protect Against Mercuric Chloride Induced Lung Toxicity In The Offspring Rat: A Histological And Immunohistochemical Study
Published in Ultrastructural Pathology, 2021
Omnia I. Ismail, Manal M.S. El-Meligy
We have suggested that the damage in the type II pneumocytes led to produce insufficient pulmonary surfactant, which trigger a rise in the surface tension, therefore the collapse of alveoli was detected in our work. It was known that the pulmonary surfactant serves to reduce the surface tension of the alveolar lining and to keep the alveoli patent enabling efficient ventilation.26 We hypothesized that prenatal mercury exposure may promote the neonatal death owing to respiratory distress syndrome generating from deficient pulmonary surfactant. Additionally, other function of the type II pneumocyte acts as a progenitor for the type I pneumocyte, which is responsible for the gas exchange and lung maintenance. This mechanism plays a critical role in injury repair and regeneration. As during pulmonary injury, the type II pneumocyte proliferates and then differentiates into the type I pneumocyte that replaces the injured one and restores the structure of alveoli.27 Therefore, we proposed that the type II pneumocyte lost their proliferative and regenerative properities and the integration between both types of pneumocytes in the present work due to HgCl2 exposure.
Histologic patterns of lung injury in patients using e-cigarettes
Published in Baylor University Medical Center Proceedings, 2020
Samreen Fathima, Haiying Zhang
The biopsies from both patients had very similar histomorphology. Sections of the transbronchial lung biopsies showed fragments of alveolar lung parenchyma with an increased number of intra-alveolar macrophages, many of which had variable-sized clear vacuoles in the cytoplasm. In addition, there was slight thickening of the alveolar septa with increased fibroblasts. Fragments of intra-alveolar granulation tissue (fibroblast plugs) consistent with an organizing pneumonia were seen in several areas (Figure 1). Patchy areas with residual intra-alveolar organizing fibrin were also seen in both cases. Type II pneumocyte hyperplasia was present, as was focal, mild acute inflammation. There was no granulomatous reaction or significant eosinophilic infiltrate. Overall, the findings indicated an organizing pattern of acute lung injury with the distinct feature of vacuolated macrophages. Acid-fast and Gomori methenamine silver stains were negative for microorganisms in both cases.