Pulmonary response to bovine albumin. A morphometric study in rats

• Escolar Castellón, J.de D. ^[1] ; Alfaro, E. ^[1] ; Roche Roche, P.A. ^[1] ; Almajano, C. ^[2] ; Gallego, B. ^[2]
  1. [1] Department of Morphological Science, Faculty of Medicine (Zaragoza)
  2. [2] Department of Surgical Pathology, Hospital <(Real y Provincial>), Zaragoza, Spain
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 9, Nº. 1, 1994, págs. 15-22
• Idioma: inglés
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  • The following hypothesis is proposed: that hypersensitivity pneumonitis (HP), experimentally induced in rats, is the cause of a thickening in the alveolar wall, a decrease in the size of the alveole, hyperplasia in the bronchus-airociated lymphoid tissue (BALT) and hypertrophy in the goblet cells. Wistar rats were classified into two different groupi, namely, non-treated animals and animals exposed to bovine albumin (BA). A morphometric study was carried out and the following variables were quantified: a) percentage of lymphocytes. neutrophils and alveolar macrophages of the bronchio-alveolar lavage (BAL); b) the interstice of the alveole, the alveolar chord length. the alveolar wall thickness and the number of alveolar macrophages with hemosiderin within its cytoplasm; c) the size of lymphatic area (LA) in BALT, the length of the lymphatic epithelium (LEp) in BALT and the percentage of goblet cells in the bronchial epithelium. The following results were obtained from the animals exposed to BA: 1) a significant increase in both lymphocytes and neutrophils of BAL, and of alveolar macrophages with hemosiderin in its cytoplasm; 2) a significant thickening of the alveolar walls and the BALT elements, which confirms the above mentioned hypothesis; 3) a significant increase in the alveolar chord and a significant decrease in the number of goblet cells of the bronchus, which contradicts the above mentioned hypothesis. The increase in alveolar macrophages with hemoiiderin is related to an increase in the capillary alveole perrneability, which, together with the variations in the BAL formula, lead us to consider the existence of an inflammation in the interstitial alveole; this interstitial alveole inflammation explains the alveolar wall thickening and the BALT hypertrophy.