Morphological studies on proliferation and desquamation of the alveolar lining epithelium in carrageenan-induced experimental pneumonia.

Mitsuhashi, Takehiro; Shimazaki, Masayoshi; Sugino, Seiki; Takeda, Tadashi; Inariba, Hiromi

doi:10.1620/tjem.140.319

Cited by 5 publications

(3 citation statements)

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“…This was observed cats and rodents. [24][25][26] The effects of carrageenin despite the reduced number of circulating leukoon lung morphology in this study are similar to cytes and suggests that either the cells were those reported previously, 25'27-3 namely, an early actively recruited into the lung (by changes in infiltration of PMN and macrophages, many of chemotaxins or adhesion molecules) or were not which phagocytosed carrageenin particles, plus cleared, perhaps because the PMN did not epithelial cell damage and basement membrane become apoptotic or because the reduced denudation, followed by Type II cell hyperplasia, number of macrophages prevented removal of…”

Section: Discussionmentioning

confidence: 99%

Effect of dexamethasone on carrageenin‐induced inflammation in the lung

Smith

Benjamin

Dewar

et al. 1995

Mediators of Inflammation

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To study the anti-inflammatory mechanisms of glucocorticoids, we have compared the effects of intratracheal carrageenin (2.5 mg) on control rats and those in which inflammation was subdued by prior dexamethasone treatment (10 mg/l in drinking water). Inflammation was maximal 48 h post-carrageenin. After dexamethasone, carrageenin caused tittle inflammation or oedema (wet lung (mg), n = 6, mean ± S.E.M.; control, 995 ± 51; carrageenin + dexamethasone, 1144 ± 83; compared with carrageenin alone, 1881 ± 198), but rats had more lung lavage neutrophils than those given carrageenin alone (PMN × 106 /lung, mean ± S.E.M.; control, 0.055 ± 0.003; carrageenin + dexamethasone, 8.54 ± 1.52; compared with carrageenin alone, 6.30 ± 1.71). Proteolysis and partial inactivation of the anti-inflammatory mediator, lipocortin 1 (Lcl), in carrageenin-instilled rats was offset in those also given dexamethasone, by increased Lc1 levels (intact Lc1 ng/ml lavage fluid, n = 4, mean ± S.E.M.; control 24 ± 6; carrageenin 15 ± 4; carrageenin + dexamethasone, 40 ± 15). Maintenance of sufficient intact (fully active) extracellular Lc1 may contribute to the actions of glucocorticoids.

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Section: Discussionmentioning

confidence: 99%

Effect of dexamethasone on carrageenin‐induced inflammation in the lung

Smith

Benjamin

Dewar

et al. 1995

Mediators of Inflammation

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“…The primary cause of respiratory bronchiolar and alveolar damages leading to emphysema may be a disrupted integrity of the lining epithelia and exposure of elastin and collagen to injurious agents. Carrageenan is said to produce necrotic areas in bronchioles (Szereda-Przestaszewska and Sieiski 1979) and also injuries of type 1 pneumocytes (Mitsuhashi et al 1983). This polysaccharide is regarded as relatively resistant to digestion by alveolar macrophages, as shown by the intracellular carrageenan retained within the phagocytic vacuoles of macrophages for as long as 500 days after the injection (Bowers et al 1980(Bowers et al , 1983.…”

Section: Discussionmentioning

confidence: 99%

“…It has also been used to induce acute and chronic inflammatory responses in the lungs of experimental animals, where it causes a transient local infiltration of polymorphonuclear leukocytes and then long-term accumulation of macrophages within the affected lobe (Velo and Spector 1973;Wachtlova et al 1975 ;Bowers et al 1980 ;Mitsuhashi et al 1983). Bowers et al (1980) found macrophage accumulation in the alveoli of some rats remaining 365 days and even 500 days after the treatment.…”

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Carrageenan-induced pulmonary emphysema of rabbit.

Mitsuhashi

Kuwahara

1989

Tohoku J. Exp. Med.

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A transbronchial injection of 0.75% carrageenan in physiologic saline induced pneumonia followed by emphysema in the insulted lobe. In the stages of pneumonia, scattered infiltration of polymorphonuclear leukocytes was seen throughout the affected lobe within a few days of treatment ; later this was replaced by the accumulation of carrageenan-laden macrophages, which lasted for one to two months. Enlargement of alveoli and alveolar ducts appeared 2 weeks to 2 months after the treatment, and pulmonary emphysema was observed at 4 months. The lobes that were not treated with carrageenan were normal in appearance during both the pneumonia and the emphysema. Morphometric analysis of the lung at 4 months showed decrease of the alveoli and/or alveolar ducts and enlargement of thier luminal spaces, also suggesting the development of emphysema. In contrast to various kinds of elastases that are known to produce emphysematous changes in animals, the elastolytic activity of carrageenan solution did not show any such effects, although in the homogenate of the lobes given carrageenan, a moderate but significant increase in the proteinase activities of alveolar macrophages are said to occur (Bowers et al. 1985). It was suggested that carrageenan-induced emphysema is a chronic disorder associated with both carrageenan toxicity and accumulated carrageenan-laden macrophages in the insulted lobes, pulmonary emphysema ; carrageenan ; rabbits ; alveolar macrophages Pulmonary emphysema is a condition of an abnormal permanent increase in size of the respiratory portion of the lung beyond the terminal bronchiole or acinus, accompanied by destructive changes (Thurlbeck et al. 1970;Dunnill 1987). However, its etiology and pathogenesis are incompletely understood. Very likely, several factors not only act together in initiating changes that lead to the disease but also contribute to its progress once it is established (Pare and Fraser 1983;Weissler 1987). The protease/antiprotease theory of pathogenesis, for which there is now considerable support, holds that alveolar wall destruction results from an imbalance between protease [mainly elastase (Snider et al. 1986)]

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