A. E. Davis

The response of the small intestine of the protein-deficient rat to infection with Nippostrongylus brasiliensis

Abstract The intestinal response of the protein-deficient Wistar rat was examined after primary infection with 1500 larvae of Nippostrongylus brasiliensis. Protein-deficient animals failed to expel N. brasiliensis after 15 days at a time when nutritionally normal animals had expelled more than 99% of the worm burden. Morphology of the small intestine of protein-deficient animals before infection showed small villi and crypt hypoplasia, followed after infection by sustained crypt hyperplasia and increased mitotic index of crypts. Protein deficiency was associated with fewer mucosal mast cells, goblet cells and intraepithelial lymphocytes. There was an impaired response of mucosal mast cells and goblet cells to infection. This could explain the deficiency of worm expulsion in these protein-deficient animals.

Role of maintenance sucralfate in prevention of duodenal ulcer recurrence

Fifty-nine patients who had duodenal ulcers that were healed following sucralfate administration in a dose of 1 g four times a day were randomly entered into a double-blind, placebo-controlled, 12-month maintenance study to determine whether sucralfate 1 g twice daily prevents recurrence of duodenal ulceration. Patients were assessed endoscopically at four, eight, and 12 months after healing or earlier if clinical relapse occurred. Of the original 59 patients, 53 showed healing with six weeks of therapy, and the remaining six patients required 10 weeks of treatment. Nine patients were subsequently lost to follow-up because of non-compliance, leaving 50 patients for the analysis, 24 who received sucralfate and 26 who received placebo. There were 10 ulcer recurrences in the sucralfate group and the ulcers in 14 (58 percent) patients remaining healed at the end of 12 months. In contrast, there were 21 recurrences in the placebo group with the ulcers in five patients (19 percent) remaining healed at 12 months. Patients who received placebo experienced recurrence more quickly than those who received sucralfate and there was no difference between the two groups in terms of symptomatic and asymptomatic recurrence. There was no alteration in serum aluminium and phosphate levels throughout the study. Smoking seemed to have no adverse effect on recurrence once initial healing had been achieved. Sucralfate is, therefore, an effective and safe maintenance treatment for duodenal ulcer disease.

The effect of protein deficiency on systemic release of rat mucosal mast cell protease II during Nippostrongylus brasiliensis infection and following systemic anaphylaxis.

Serum rat mucosal mast cell protease II (RMCPII) was measured in protein‐deficient rats to assess mucosal mast cell (MMC) activation during primary infection with the nematode, Nippostrongylus brasiliensis, and during systemic anaphylaxis produced by Nippostrongylus antigen in immune animals. In the first study, serum RMCPII increased 4‐fold by day 15 after infection. By day 20, serum RMCPII continued to rise in protein‐deficient animals, but decreased in nutritionally normal animals. This was associated with impaired worm rejection in protein‐deficient rats. During systemic anaphylaxis, serum RMCPII was elevated in three groups of protein‐deficient rats on 6%, 8% and 10% low protein diets and in nutritionally normal rats. All protein‐deficient rats exhibited 3 to 7‐fold less mucosal permeability of the small intestine to Evans blue dye injected intravenously compared to nutritionally normal animals following anaphylactic stimulation. These results demonstrated that MMC are activated during infection in protein deficiency, and suggest that reduced MMC function does not explain delay in worm expulsion. Impaired mucosal anaphylaxis in protein deficiency could not be attributed to a failure of MMC response.