Cell biology of laryngeal epithelial defenses in health and disease: preliminary studies.

Esophageal epithelium has intrinsic antireflux defenses, including carbonic anhydrases (CAs I to IV) that appear to be protective against gastric reflux. This study aimed to investigate the expression and distribution of CA isoenzymes in laryngeal epithelium. Laryngeal biopsy specimens collected from the vocal fold and interarytenoid regions were analyzed by Western blotting and immunofluorescence. Carbonic anhydrases I and II were expressed by the majority of samples analyzed. In contrast, CA III was differentially expressed in the interarytenoid samples and was not detected in any vocal fold samples. The expression of CA III was increased in esophagitis as compared to normal esophageal tissue. Carbonic anhydrase I and III isoenzymes were distributed cytoplasmically in the basal and lower prickle cell layers. The laryngeal epithelium expresses some CA isoenzymes and has the potential to protect itself against laryngopharyngeal reflux. Laryngeal tissue may be more sensitive to injury due to reflux damage than the esophageal mucosa because of different responses of CA isoenzymes.

Fluid phase endocytosis within buccal mucosal cells of alcohol misusers.

The structure of the oral mucosa is now well characterised, although studies on oral epithelial cell function have received less attention. The aims of this study were to see whether endocytosis could be demonstrated in cells from oral smears and if so, to assess the effect of chronic high alcohol intake on such uptake. Buccal mucosal smears were collected from 135 patients (91 non- or social drinkers, and 44 patients with harmful alcohol use). Name, age, sex, and alcohol history (for alcohol problem patients) were recorded. Cell suspensions were incubated in a solution of bovine serum albumin (BSA)-coated fluorescently labelled latex microspheres (0.02 micron diameter) in Ham's F-10 culture medium for 1 h at 37 degrees C as a marker of fluid phase endocytosis. Uptake of microspheres was confirmed by confocal microscopy, and mean endocytosed fluorescence levels determined by flow cytometry. A repeat smear from 11 of the alcohol patients was taken 9-14 days later. Endocytosis was significantly reduced in both male (P < 0.01) and female (P < 0.01) alcohol problem patients compared to controls. Units of alcohol consumed and cigarettes smoked per day did not show a dose-response correlation with endocytosis in the alcohol problem patients. Apparent abstinence from alcohol had no further effect on endocytic uptake at days 9-14. This study shows that normal oral squamous cells removed as buccal smears readily endocytose fluorescent microspheres and that this capacity can be affected by alcohol. Chronic high alcohol intake would appear to down regulate endocytosis in buccal cells even up to 14 days of abstinence. This may have implications for the pathogenesis of oral mucosal disorders in long-term users.