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Airway Repair and Adaptation to Inhalation Injury
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
S. F. Paul Man, William C. Hulbert
Ozone is less soluble than SO2 (Perry, 1950) and it is a stronger oxidizing agent. Accordingly, the site and type of airway epithelial injury caused by ozone would be anticipated to be different from those caused by SO2. Because of its presence in the atmosphere, it has received considerable attention (Castleman et al., 1973, 1980; Stephens et al., 1973, 1974; Boorman et al., 1980; Eustis et al., 1981; Last et al., 1984). Both long- and short-term studies have been carried out, in a number of animal species, and under different laboratory conditions. In general, while the upper airways are undoubtedly affected, the epithelium of the terminal bronchiole and alveoli shows the most profound morphologic damage. Further, the type I pneumocyte is the most sensitive alveolar cell to inhalation injury and the type II and cuboidal nonciliated bronchiolar cells act as the stem cells for repair (Castleman et al., 1980).
Comparative Aspects of Pulmonary Surfactant
Published in Jacques R. Bourbon, Pulmonary Surfactant: Biochemical, Functional, Regulatory, and Clinical Concepts, 2019
Cells with the characteristic features of type I and type II pneumocytes have also been observed in the avian lung. They are, however, not associated in the same pulmonary structure as the alveolus of the mammalian lung. While type II pneumocytes form a cuboidal epithelium which lines tertiary bronchi and atria, i.e., air-conducting portions, type I pneumocyte is the exclusive cell type of air capillaries (Figure 3). The presence of osmiophilic inclusions in avian lung was reported early.26 There appear to exist two distinct types of osmiophilic inclusions in the lung of birds. One is designated the osmiophilic inclusion body (OIB)27 or OIB type A28 and the other is designated avian inclusion body27 or OIB type B.28 The former, resembling the multilamellar bodies of mammalian type II pneumocytes, is a round, electron-dense inclusion averaging 0.5 μm in diameter containing lamellar whorled structures. The latter is a very electron-dense, rod-shaped body about 1 μm in width and 3 to 4 μm in length which contains parallely arranged lamellae of 5 to 10 nm in thickness. Both types are found in the same cell. They are both considered to contribute to the formation of the laminated film lining the respiratory epithelium which appears to represent surfactant material.29–32
Histopathology of interstitial lung disease: A pattern-based approach
Published in Muhunthan Thillai, David R Moller, Keith C Meyer, Clinical Handbook of Interstitial Lung Disease, 2017
Angela M Takano, Junya Fukuoka, Kevin O Leslie
This phase begins in the second week following a single injury and lasts for 1 or 2 weeks. It consists of marked type II pneumocyte proliferation beneath the hyaline membranes, and differentiation toward type I pneumocytes in order to cover up the denudation that the alveolar surfaces suffered during the exudative phase, while ‘pushing-off’ some hyaline membranes into the alveolar lumen. In some instances, however, the epithelium incorporates the hyaline membranes into the interstitium, where they can participate in a fibrotic process (6). Type II pneumocyte hyperplasia can also be accompanied by marked squamous metaplasia, so extreme as to simulate a malignancy (Figure 2.3).
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).
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.
Phyllanthin and hypophyllanthin from Phyllanthus amarus ameliorates immune-inflammatory response in ovalbumin-induced asthma: role of IgE, Nrf2, iNOs, TNF-α, and IL’s
Published in Immunopharmacology and Immunotoxicology, 2019
Wei Wu, Yinfang Li, Zelin Jiao, Li Zhang, Xiaohua Wang, Rui Qin
Figure 7(A) represents the normal structure of nuclei and cytoplasm from the lungs of normal animals. It showed the presence of normal architecture of type II pneumocyte, bronchial epithelial alveoli with the nucleus. However, the presence of vacuolization and phagocytes were evident in the lungs of normal animals (Figure 7(A)). AHR control rat displayed extensive vacuolization of the alveolar type II cells, inflammatory infiltration and irregular shrunken nucleus with abnormal cytoplasm (Figure 7(B)). The epithelium is showing ballooning of the endothelial cell in the capillary lumen with the presence of lamellar bodies in lungs of AHR control rats. The thickness of interstitial septa and the nuclear membrane was increased. It showed the presence of vesicular cytoplasm, electron-dense mitochondria and pyknosis of the alveolar epithelial cell (Figure 7(B)). Lung tissue from montelukast (10 mg/kg) administered rats showed invaded nuclear membrane with the presence of cytoplasmic vesicular granules in vesicles (Figure 7(C)). Lung tissue from P. amarus (200 mg/kg) treated rat showed reconstructed bronchial epithelial cells with narrow septa, mucous secreting endothelial cells, the presence of mild intracellular fibrosis, polymorphic mononuclear cell infiltration, and vesicular cytoplasm (Figure 7(D)).