Background: Candida albicans resides on epithelial surfaces as part of the physiological microflora. However, under certain conditions it may cause life-threatening infections like Candida sepsis. Human β-defensins (hBDs) are critical components of host defense at mucosal surfaces and we have recently shown that hBD-2 and hBD-3 are upregulated in Candida esophagitis. We therefore studied the role of Candidate signalling pathways in order to understand the mechanisms involved in regulation of hBD-expression by C. albicans. We used the esophageal cell line OE21 and analysed the role of paracrine signals from polymorphonuclear leukocytes (PMN) in an in vitro model of esophageal candidiasis.

Development of pouchitis correlates with decreased defensin expression in ulcerative colitis in addition to high expression of cytokines. The low incidence of pouchitis in FAP pouches correlates with increased expression of hBD-1 beta-defensin in association with low cytokine levels.

The differing expression of AMPs in HPV-infected, compared with noninfected, vulvovaginal biopsy samples suggests that these peptides are important in the local immune response. Curiously, hBD-1 shows a significant induction whereas RNase7 does not, which suggests differing regulation of AMPs over the course of bacterial and viral infections.

This study examined the inhibitory mechanism of galanin, a 29 amino acid polypeptide on pancreatic enzyme secretion in anaesthetised rats, isolated pancreatic acini, and lobules. Urethane anaesthetised rats with pancreatic fistulas pretreated with 3-0-methylglucopyranose (500 mg/kg/h) were stimulated with an intravenous bolus of 2-deoxyglucose (2-DG) (75 mg/kg). Maximal amylase secretion was mean (SEM) 274 (19 (Gut 1993; 34: 1616-1621 Galanin, a 29 amino acid peptide, was first isolated from porcine intestinal mucosa by Tatemoto et al using a method that detects its C-terminal amide structure.' The name was derived from its N-terminal amino acid glycine and the C-terminal amino acid alanine. Galanin is widely distributed in the neurons of the central nervous system and the gut and coexists with norepinephrine, serotonin, y-amino butyric acid, vasopressin, cholecystokinin (CCK) and acetylcholine.2'-The localisation and the coexistence with these neurotransmitters strongly suggests that galanin plays an important part in the modulation of neural transmission. In the pancreas galanin immunoreactive nerve fibres have been detected in several species, only the intrapancreatic abundance and distribution varies slightly among them.9 In the rat galanin immunoreactive nerve fibres are located around blood vessels and scattered in the exocrine pancreatic parenchyma, occasionally in the islets. Therefore, in this study we investigated the hypothesis that galanin inhibits pancreatic enzyme secretion by presynaptic modulation of acetylcholine release. To test this hypothesis we examined the effect of galanin (a) on 2-deoxyglucose (2-DG) stimulated amylase release in anaesthetised rats, (b) on CCK8 and carbachol stimulated amylase release from isolated pancreatic acini devoid of neural elements, (c) on the sodium channel activator veratridine stimulated amylase release from pancreatic lobules contain-

Epithelialization and local production of antimicrobial peptides in anal fistulas serve as defence mechanisms to prevent local and systemic infection by microbes from faeces passing through the fistula tract.