Biomedical subjects

G H Curtis

Publications and source records attributed to G H Curtis.

9 recordsLinked to original sources

PubMed1992

Macromolecular transport by rat gastric mucosa.

We previously demonstrated that the stomach is capable of mounting a type I hypersensitivity reaction to luminal antigen challenge. These findings imply that antigenically intact macromolecules cross the gastric mucosa. To test this hypothesis, rat gastric mucosa was mounted in Ussing chambers, and bovine serum albumin (BSA, 0.5 mg/ml) and 125I-labeled BSA (10 microCi) were added to mucosal fluids. After equilibration, serosal fluids were sampled for two 30-min periods, and fluxes of immunologically intact BSA (determined by an enzyme-linked immunosorbent assay) and total BSA (125I-BSA) were calculated under basal conditions and in the presence of NaF and colchicine, and at 4 degrees C. Additional experiments examined macromolecular permeability in sensitized-challenged tissues. Immunologically intact BSA (21.3 +/- 4.5 ng.30 min-1.cm-2) crossed the gastric mucosa as approximately one-fourth of the total BSA flux (78.2 +/- 7.5 ng.30 min-1.cm-2). The uptake of immunologically intact BSA was significantly reduced by NaF, an inhibitor of ATP production and endocytosis; colchicine, which inhibits polymerization of cytoskeletal microtubules; and at 4 degrees C, a general metabolic inhibitor. The transmural passage of antigen was not significantly altered by immunoglobulin E-mediated anaphylaxis. These findings indicate that intact protein antigens cross the gastric mucosa by an active, energy-dependent mechanism that uses the microtubular network.

Anaphylaxis↗

PubMed1990

Effect of acute Yersinia enterocolitica infection on small intestinal ultrastructure.

The purpose of this study was to assess the jejunal and ileal brush border injury caused by Yersinia enterocolitica and to correlate these alterations with functional abnormalities. Weanling rabbits infected with 10(10) organisms of a human pathogenic Y. enterocolitica strain were compared with control and pair-fed, sham-treated animals. On day 6, infection resulted in a diffuse decrease in brush border enzyme activities in the small intestine and villus atrophy and crypt hyperplasia in the ileum. By day 14, ileal architecture and jejunal disaccharidases had returned to normal, but enzyme abnormalities persisted in the ileum. Ultrastructural studies showed decreased brush border surface area in the jejunum and ileum on day 6 and in the ileum on day 14 of infection. Abnormalities of brush border function caused by infection correlated with the changes in microvillus surface area. In pair-fed animals on day 6, brush border surface area was slightly decreased in the ileum but increased in the jejunum, suggesting that the brush border injury resulted from infection rather than from malnutrition alone. The findings indicate that Y. enterocolitica inflicts a diffuse brush border injury that is in keeping with the generalized defect in brush border enzyme activity and transport function.

Abscess↗

PubMed1990

Intestinal anaphylaxis in the rat. Effect of chronic antigen exposure.

The effect of chronic dietary antigen challenge on the intestine was examined in sensitized rats. Three groups of Hooded-Lister rats were studied: animals sensitized to egg albumin; sham-sensitized animals; and unmanipulated controls. In sensitized rats, serum immunoglobulin E titers to egg albumin were greater than or equal to 1:64, whereas control and pair-fed rats showed no response. Sensitized rats received egg albumin 1 mg/ml in drinking water and rat chow ad libitum. Pair-fed animals also received egg albumin but were pair-fed with sensitized animals. Controls received water and rat chow ad libitum. Chronic antigen challenge resulted in reduced food intake and weight gain in sensitized animals. When the rats were killed after 9 days of antigen exposure, proximal intestine from experimental animals showed decreased disaccharidase activity, brush-border microvillus surface, area, and villus height. Crypt depth and enterocyte migration rate were increased. Mucosal mast cell involvement was suggested by mast cell proliferation, evidence of mast cell degranulation, and increased serum rat mast cell protease II levels. At the time of death, only sensitized jejunum demonstrated an increase in short-circuit current in Ussing chambers in response to antigen challenge. The findings indicate that chronic antigen exposure leads to intestinal injury, reduced food intake, and diminished weight gain.

Anaphylaxis↗

PubMed1976