concanavalin-a has been researched along with Intestinal-Diseases* in 4 studies
4 other study(ies) available for concanavalin-a and Intestinal-Diseases
Article | Year |
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The effects of lectins on indomethacin-induced small intestinal ulceration.
Growth factors, such as epidermal growth factor and keratinocyte growth factor, have considerable therapeutic potential for repairing mucosal injury in the intestine when given systemically. Recently, several lectins have been shown to have trophic effects on the intestine when given orally. We examined the effects of phytohaemagglutinin (PHA) and concanavalin A (Con-A) on indomethacin-induced intestinal injury in rat. Five-week-old rats were randomized to four groups (n=5), and intestinal injury was induced by indomethacin injection in three of these groups. Elemental diet (ED) feeding was then commenced. The groups were thus ED feeding/indomethacin untreated (control group), ED feeding/indomethacin treated (ED group), 0.1% PHA-supplemented ED feeding/indomethacin treated (PHA group) and 0.1% Con-A-supplemented ED feeding/indomethacin treated (Con-A group). After 7 days of feeding, macroscopic inflammatory scores, mucosal permeability, myeloperoxidase (MPO) activities and cell proliferation were determined. Macroscopic inflammatory scores, mucosal permeability and MPO activities were significantly lower in both lectin groups than that in control group. Twenty-four hour excretion rate of phenolsulphonphthalein was significantly lower in both lectin groups than that in ED group. Cell proliferation of the small intestine was significantly increased by both lectins. Lectin supplementation can induce ulcer healing following indomethacin-induced damage. Topics: Animals; Cell Division; Concanavalin A; Food, Formulated; Indomethacin; Intestinal Diseases; Intestinal Mucosa; Intestine, Small; Lectins; Male; Permeability; Peroxidase; Phytohemagglutinins; Rats; Rats, Sprague-Dawley; Ulcer | 2003 |
Deficient cell-mediated cytotoxicity and hyporesponsiveness to interferon and mitogenic lectin activation by inflammatory bowel disease peripheral blood and intestinal mononuclear cells.
Intestinal mononuclear cells are poor mediators of spontaneous and antibody-dependent cellular cytotoxicity. In this study, we found that both interferon and mitogenic lectins were able to induce increased levels of cell-mediated cytotoxicity by intestinal mononuclear cells. Intestinal mononuclear cells from patients with inflammatory bowel disease exhibited hyporesponsiveness to cytotoxic activation by interferon or lectins compared with control intestinal mononuclear cells. Peripheral blood mononuclear cells from patients with Crohn's disease exhibited deficient spontaneous and antibody-dependent cytotoxicity that could be partially reversed by interferon or mitogenic lectins. These studies demonstrate that exogenous agents or endogenous factors can induce deficient intestinal and peripheral blood cytotoxic effector cells from inflammatory bowel disease patients to become active. In comparison with control cells, however, intestinal and peripheral blood mononuclear cells from inflammatory bowel disease patients are not only deficient in cytotoxic capabilities but also are hyporesponsive to interferon and lectin activation. Topics: Antibody-Dependent Cell Cytotoxicity; Concanavalin A; Crohn Disease; Cytotoxicity, Immunologic; Humans; Inflammation; Interferon Type I; Intestinal Diseases; Intestines; Killer Cells, Natural; Lymphocyte Activation; Monocytes; Pokeweed Mitogens | 1986 |
Specificity of the suppressor cell activity of intestinal lymphocytes.
Experiments were designed to examine the functional characteristics of lymphocytes harvested from the human intestine. Lymphocytes were harvested from the intestines of patients undergoing intestinal resection for a variety of gut disorders. The mitogenic and allogeneic responses of gut lymphocytes were found to be comparable with the response of peripheral blood lymphocytes. Intestinal suppressor cell activity was found to be more specific against other intestinal lymphocytes than peripheral mononuclear cells. The regulation of the intestinal immune response in various bowel disorders may be determined at a local level to a greater degree than had been previously appreciated. Topics: Antibody Specificity; Cells, Cultured; Concanavalin A; Humans; Intestinal Diseases; Intestines; Lymphocyte Activation; Phytohemagglutinins; Pokeweed Mitogens; T-Lymphocytes, Regulatory | 1983 |
Mucotractive effect of lectin.
The jackbean lectin concanavalin A caused hypersecretion of mucus in the human nose and the rat jejunum, and histology of the latter demonstrated increased emptying of goblet cells. This "mucotractive" effect has implications for the fibre hypothesis and might be therapeutically useful in patients with cystic fibrosis. Topics: Animals; Colic; Concanavalin A; Female; Flatulence; Humans; Intestinal Diseases; Intestinal Mucosa; Jejunum; Male; Mucus; Nasal Mucosa; Rats; Rhinitis; Stimulation, Chemical | 1978 |