Regulation of parotid salivary proteins by glucocorticoids.

Previous studies have indicated that adrenal-intact rats treated for one week with pharmacological doses of the synthetic glucocorticoid, dexamethasone, show a significant reduction in the proportion of proline-rich proteins and an increase in the proportion of amylase in rat parotid saliva (Johnson et al., 1987). In order to understand more fully the role of glucocorticoids in the regulation of salivary proteins, we performed bilateral adrenalectomies on groups of rats. Some of the adrenalectomized rats were treated with replacement-level doses of the synthetic glucocorticoid, dexamethasone. The food intake was monitored daily for both groups, and sham-operated pair-fed controls were included so that the effects of alterations of food intake could be separated from those of the experimental procedures. After eight to 12 days, uniformly stimulated parotid saliva was collected from these animals as well as from sham-operated controls fed ad libitum. The volume of saliva collected in 30 min was recorded, and the saliva samples were analyzed for concentration and composition of protein. Although the volume of saliva was not affected, parotid saliva collected from adrenalectomized rats exhibited a two-fold greater proportion of proline-rich proteins and reductions in other major secretory proteins: DNase, Fraction I, and Fraction V. The parotid gland secretory granules of adrenalectomized rats were more electron-lucent than in the ad libitum-fed controls. Treatment of adrenalectomized rats with dexamethasone largely prevented the changes in salivary protein composition as well as the alterations in secretory granule morphology.(ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of salivary proteins.

Previous studies have shown that several factors--such as alloxan-induced diabetes, adrenalectomy, or removal of the thyroid-parathyroid gland complex--can influence the flow rate, protein concentration, and protein composition of rat parotid saliva. The present study was undertaken to explore further the influence of glucocorticoids and thyroxine on rat parotid saliva in hormonally intact animals. As compared with untreated animals, adult male rats treated with 10 micrograms dexamethasone per 100 g body weight for eight days demonstrated a 75% reduction in volume of parotid saliva secreted in response to a uniform stimulus. The protein concentration of the saliva was increased three-fold. Sodium dodecyl sulfate polyacrylamide gel electrophoresis showed relative decreases in acidic and basic proline-rich proteins and in a protein identified as Fraction V, while amylase was increased. The electron microscopic appearance of the granules was markedly different from that of the control, in that the granules exhibited an electron-dense periphery and core, with the remainder of the granule having an electronlucent appearance. In contrast, rats treated for eight days with 20 micrograms thyroxine per 100 g body weight exhibited a 50% increase in volume of saliva collected in response to a secretory stimulus. Although the concentration of protein was not different from that of the control, gel electrophoresis showed relative increases in acidic and basic proline-rich proteins and a decrease in Fraction V. Amylase was unchanged. The secretory granules of thyroxine-treated rats were electronlucent and amorphous. The granules appeared to coalesce within the cell.(ABSTRACT TRUNCATED AT 250 WORDS)

Zinc deficiency-induced changes in rat parotid salivary proteins.

This study was undertaken to determine the effects of zinc deficiency on rat parotid salivary proteins. Male rats were fed a pelleted diet containing either 40 ppm Zn (ad libitum- and pair-fed control groups) or 0.9 ppm Zn (zinc-deficient group) for a period of 4 weeks. At the time they were killed, stimulated parotid saliva was collected and analyzed for concentration and composition of secretory protein. In addition, gland specimens were examined ultrastructurally, and liver and serum samples were assayed for zinc concentration. The zinc-deficient group exhibited retarded body growth, decreased appetite and significantly lower serum and liver zinc concentrations. The most significant finding in the saliva of the deficient animals was the marked reduction in acidic proline-rich proteins. Parotid gland secretory activity also seemed reduced. Morphologically, distinctive secretory granules were observed in the acini of the deficient animals. The altered composition of salivary secretory proteins coupled with a diminished flow rate may, in part, be responsible for the increased susceptibility to dental caries in zinc-deficient rats.

The effects of severe protein-calorie malnutrition on antibacterial defense mechanisms in the rat lung.

Protein-calorie malnutrition (PCM) impairs systemic immunity in humans and animals, but its effects on regional defense mechanisms in the lung are not clear. Therefore, we investigated lung phagocytic antibacterial defenses in vivo and in vitro in an animal model of PCM. Matched groups of weanling rats consumed Isocaloric diets containing either 0.8% (PCM) or 24% protein (Control, C). A third group of animals was fed the C diet in restricted amounts to match the daily caloric intake of the PCM animals (pair-fed control, PF). After 4 wk on the diet, PCM animals were hypoproteinemic, hypoalbuminemic, and anemic and had depressed systemic cell-mediated immunity. In vivo, the lung clearance rate of Listeria monocytogenes was markedly delayed in PCM animals (% bacterial recovery at 9 days, mean +/- SE:PCM = 120 +/- 25.1; PF = 5.2 +/- 3.0; C = 0.6 +/- 0.6; p less than 0.001 for PCM versus C). Only 36% of the PCM animals survived for 9 days after Listeria exposure, whereas more than 94% of the C and PF animals survived (p less than 0.01). Recruitment of macrophages to the lungs of PCM animals after Listeria aerosolization was markedly impaired compared with that in the PF and C animals (p less than 0.001). By contrast, lung clearance rates of 2 pyogenic organisms, Staphylococcus aureus 502a and Pseudomonas aeruginosa 177, were similar in all groups. In vitro, alveolar macrophage chemotaxis toward zymosan-activated serum, and microbicidal activity against Staphylococcus epidermidis were also similar in all groups of animals. Our findings indicate that in the rat, PCM impairs the pulmonary clearance of L. monocytogenes, and that this defect is associated with impaired macrophage recruitment to the lung after Listeria inhalation.(ABSTRACT TRUNCATED AT 250 WORDS)