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A Ferguson

Publications and source records attributed to A Ferguson.

At least 343 records · Page 19Linked to original sources
PubMed1970

Coeliac disease.

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Celiac Disease↗
PubMedDate not supplied

Effects of local delayed hypersensitivity on the small intestine.

There are many T and B cells in the small intestinal mucosa and local T cell immunity could have a role both in protective immunity and as a cause of disease (i.e. hypersensitivity). This latter aspect has been investigated by using several animal models to assess the effects of local delayed hypersensitivity on the structure and function of the small intestine. Heterotopically transplanted grafts of fetal small intestine in mice (isografts and allografts) have been examined by conventional histology, scanning and transmission electron microscopy, by making direct measurements of villi, crypts, and lymphoid cell infiltrate, and by counting the number of mitoses per crypt. This cell-mediated immune reaction causes lymphocyte infiltration which is most marked in the lamina propria, hyperplasia of the crypts of Lieberkühn, increased cell loss with villous atrophy and a flat surface, but the individual enterocytes appear fairly normal. Graft-versus-host disease cause exactly the same changes in structure and in cell kinetics as does rejection. However, crypt hyperplasia has been found to precede villous atrophy by several days. Preliminary experiments on local contact hypersensitivity suggest that intraluminal injection of oxazolone in the gut of sensitized mice also produces villous atrophy and crypt hyperplasia. It is postulated that these effects are likely to be produced via lymphokines: by an 'enteropathic' factor which damages the lamina propria and basement membrane, and a factor which is mitogenic for crypt stem cells. In mice infected with Giardia lamblia, crypt hyperplasia and lymphocyte infiltration of the epithelium are present and there is accelerated epithelial cell turnover. In rats infected with Nippostrongylus brasiliensis, the flat mucosa has been shown to be due to the thymus-dependent immune response and not directly to the damage produced by the parasite itself. A common factor in the variety of conditions associated with villous atrophy and crypt hyperplasia may well be a local cell-mediated immune reaction to food, microbial, parasite or other antigens which causes changes in enterocyte turnover rate and malabsorption.

Animals↗
PubMedDate not supplied

Association of maturation of the small intestine at weaning with mucosal mast cell activation in the rat.

Maturation of the small intestine at weaning has some features in common with immunological reactions involving the gut mucosa. Mucosal mast cell (MMC) activation is a prominent feature of both IgE and cell-mediated mucosal immune responses. MMC activation was therefore studied during the weaning period by measurement of rat mucosal mast cell protease II (RMCPII) release into the systemic circulation as well as MMC counts and jejunal RMCPII content. Maturation of the small intestine was measured by changes in villus and crypt length, and in crypt cell production rate (CCPR). At 3 weeks of age, serum RMCPII increased 17-fold and MMC showed features of degranulation. At the time of weaning (2-4 weeks), villus and crypt length and CCPR increased progressively to adult values. After weaning, serum RMCPII declined slowly to normal adult levels and MMC regained a normal appearance. This study showed a close association between MMC activation and maturation of the small intestine during the weaning period.

Animals↗