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PubMed1984

Age-related decline of lymphoid-tissue components in the oral mucosa of the lip, cheek and soft palate of Macaca fascicularis.

In three mature monkeys (Macaca fascicularis; 3.5 +/- 0.3 kg in weight), the labial, buccal and soft-palate mucosae were examined morphologically and stereologically. Using fixation by perfusion, standardized methods of tissue preparation and morphometric analysis at the light-microscopic level, the gross dimensions (i.e., epithelial thickness, width of combined lamina propria/submucosa) and the volumetric composition of the oral mucosae were estimated and compared with those of young animals examined previously. The data show (1) an age-related decline in the volume and prevalence of organized lymphoid tissue (i.e., lymphoid follicles associated with secretory ducts), (2) a stable plasma-cell density in the interglandular connective tissue, and (3) an increase of glandular tissue in mature versus young animals. It is suggested that the lymphoid follicles associated with secretory ducts, providing for plasma-cell generation, mirror the tonsillar lymphoid tissue declining after puberty.

Aging↗
PubMed1989

Prostaglandin E2 prevents diclofenac-induced enhancement of histamine release and inflammation evoked by in vivo challenge with compound 48/80 in the hamster cheek pouch.

Based on observations obtained by the use of intravital microscopy, we report that prostaglandins (PGs) can exert inhibitory effects on mast cell-dependent inflammation. Thus, the PG-synthesis inhibitors diclofenac and indomethacin potentiated extravasation of plasma evoked by challenge with the mast cell secretagogue compound 48/80. Although the plasma leakage induced by compound 48/80 was in large mediated by histamine, neither diclofenac nor indomethacin potentiated the plasma leakage caused by exogenous histamine. These findings indicated that endogenous PGs inhibited the mast cell-dependent reaction at the level of mediator release. This mode of action was confirmed, as diclofenac was found to enhance the in vivo release of histamine that ensued challenge with compound 48/80. Moreover, the enhancement of the response to compound 48/80 observed after diclofenac treatment was prevented by local administration of PGE2 (30 nM). This inhibition included both the histamine release and the plasma leakage. In addition, diclofenac enhanced the leukocyte emigration after compound 48/80 challenge, and PGE2 reversed also this effect, suggesting that endogenous PGs (e.g. PGE2) also inhibited the release of chemotactic mediators.

Animals↗