Biomedical subjects

E C Lucey

Publications and source records attributed to E C Lucey.

58 records · Page 4Linked to original sources

PubMedDate not supplied

Resistance of hamster bronchiolar epithelium to neutrophil elastase: investigation by cell surface lectin cytochemistry.

An intratracheal instillation of human neutrophil elastase (HNE) causes accumulation of an excess number of secretory granules in the epithelial secretory cells lining the hamster bronchus. This chronic lesion, which we refer to as secretory cell metaplasia (SCM), is not seen in the trachea or bronchioles. Because luminal cell surface lectin binding is much higher in the trachea than in the bronchus, we concluded that tracheal resistance may be due to a protective glycoconjugate coat. In the present ultrastructural study, we analyzed the lectin-binding capability of bronchiolar epithelial cells to determine whether their luminal cell surface glycoconjugate layer is similar to tracheal epithelial cells. None of the six ferritin-conjugated lectins showed higher binding in bronchioles compared to the bronchus, suggesting that a high level of surface oligosaccharides is not necessary for resistance to the metaplastic effects of HNE. HNE caused a significant reduction in bronchiolar surface binding of the gold-labeled, secretory cell-specific lectin, Helix pomatia agglutinin. The principal granulated secretory cell type in bronchioles was ultrastructurally similar to a form of bronchial Clara cell that converts to a mucous cell phenotype in response to HNE. The results suggest that absence of bronchiolar SCM is not attributable to a protective layer of cell surface oligosaccharides, a lack of cellular contact by HNE, or the presence of a morphologically distinct population of epithelial cells in bronchioles.

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PubMedDate not supplied

Changes in the carbohydrate content of airway epithelium induced by human neutrophil elastase in the hamster.

Hamster airway epithelial secretory cells were investigated by light and electron microscopic cytochemistry to study possible changes in their carbohydrate content induced by human neutrophil elastase (HNE), an agent known to cause replacement of Clara cells by mucous cells in hamster bronchi. Characterization of secretory cell carbohydrates by the AB/PAS, PA-TCH-SP, HID-TCH-SP, and LID-TCH-SP sequences indicated the existence of periodate-reactive acidic glycoconjugates, but the absence of sulfated or carboxylated glycoconjugates in both treated and control animals. Differences were seen in the quality and quantity of historeactive carbohydrates throughout various regions in the lower respiratory tract. This was especially evident in the HNE-treated animals. It is concluded that the HNE-induced expression of the mucous cell phenotype is associated with an increase in the amount of neutral and acidic nonsulfated and noncarboxylated polysaccharides stored in the secretory granules of these cells.

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PubMedDate not supplied

Elastase causes secretory discharge in bronchi of hamsters with elastase-induced secretory cell metaplasia.

A single intratracheal instillation of human neutrophil elastase (HNE) into hamsters causes granule discharge from bronchial secretory cells followed by marked accumulation of granules, visible by light microscopy at 21 days and persisting through 18 months. To determine whether persistence of this secretory cell metaplasia (SCM) is due to inability of the metaplastic secretory cells to secrete their granules, hamsters having HNE-induced SCM were challenged with the potent secretagogue HNE. Four groups of 10 hamsters each received 300 micrograms HNE intratracheally. Twenty-one days later, hamsters were intratracheally treated with HNE or saline; the groups were designated HNE-HNE and HNE-SAL, respectively. Hamsters were killed 2 h or 21 days following the second treatment. Using light microscopy, nucleated epithelial cells were counted in plastic sections of the left main intrapulmonary bronchus. Cells were classified as ciliated (C), basal (B), indeterminate (IN), or secretory. Secretory cells were subcategorized as S0 (0 granules), S1 (1-4 granules), S2 (> or = 5 granules with intervening cytoplasm), and S3 (abundant granules completely filling the cytoplasm). At 2 h, S3 cell frequency in the HNE-HNE group was 13.0 +/- 2.2 (% mean +/- SE), significantly lower than in the 2 h HNE-SAL group (31.1 +/- 4.5). Concomitantly, higher cell frequencies were seen in the other secretory categories of the HNE-HNE group compared to the HNE-SAL group; S2 17.1 +/- 1.9 compared to 9.4 +/- 1.9, S1 2.4 +/- 0.4 compared to 1.1 +/- 0.5, and S0 2.4 +/- 0.5 compared to 1.1 +/- 0.5, respectively. The S3 cell frequency of the 21-day HNE-HNE group was 25.4 +/- 4.7, increased significantly compared to the 2 h HNE-HNE group; this change was concomitant with significant decrease in the frequency of the S0 secretory cells. Cell frequencies of C, B, and IN were not affected by treatment or time. It is concluded that metaplastic secretory cells discharge their granules in response to HNE; SCM returns to its original state after HNE rechallenge; persistent SCM is not due to the inability of metaplastic secretory cells to discharge their granules.

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PubMedDate not supplied

Hypercapnic ventilatory response in unanesthetized normal hamsters.

In order to measure the hypercapnic ventilatory response (HCVR) in experimental animals, it is desirable that the animals be unanesthetized and unrestrained. In the present study, we used a barometric chamber to measure steady state HCVR of hamsters with chronic cannulation of their aortas. In 16 hamsters, the mean (+/- SD) of HCVR, defined as changes in ventilation divided by changes in Paco2 (range 53-73 mmHg), was 10.1 +/- 4.9 ml X min-1 X mmHg-1. The rise in ventilation during CO2 inhalation at low concentrations was due to a rise in mean inspiratory flow and tidal volume. As inhaled Pco2 increased, frequency of breathing increased because expiratory time fell progressively. Inspiratory time rose slightly with small increases in inhaled CO2, but returned to baseline values as the concentration of inhaled Pco2 increased. These changes in ventilation and its components appear to resemble those found in the unanesthetized cat and in man, but are somewhat different from those found in the rat.

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