Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021390 (inflammatory bowel disease)
 23,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have developed an enzymatic technique for isolating human intestinal mucosal lymphoid cells. This method was found to be superior to mechanical methods in regard to cell yield and survival. It is based on treating mucosa with serum-free solutions containing collagenase and deoxyribonuclease, followed by isolating the lymphoid cells through centrifugation steps involving fetal calf serum and ficoll-hypaque. Exposure of peripheral blood lymphocytes to the components of the enzymatic solution did not appreciably alter their uptake of tritiated thymidine in the presence or absence of mitogens. Application of the method to derive lymphoid cells from Crohn's disease, ulcerative colitis, and normal intestinal mucosa has shown that gut mucosal lymphocytes from inflammatory bowel disease (1) exceed the number of those from normal mucosa by a factor of 3 to 5; (2) show different degrees of tritiated thymidine uptake, spontaneously and in response to mitogens, depending upon the time they are harvested during the dissociation process; (3) are better stimulators than responders in the allogeneic mixed lymphocyte reaction; (4) generate suppressor cell activity comparable to that of peripheral blood lymphocytes; (5) cannot, in contrast to peripheral blood lymphocytes, generate antibody-dependent cell mediated cytotoxicity; and (6) produce an average of 5 times more IgM than equal numbers of peripheral blood lymphocytes.
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PMID:Gut mucosal lymphocytes in inflammatory bowel disease: isolation and preliminary functional characterization. 15 97

Immunologic characteristics of intestinal mucosal lymphoid cells from patients with inflammatory bowel disease and controls have been compared. Mononuclear cells isolated by enzymatic means from intestinal tissues involved with inflammatory bowel disease were present in greater numbers, with increased proportions of macrophages and B-lymphocytes, particularly cells bearing intrinsic membrane immunoglobulin G. Synthesis of immunoglobulin G, measured by radioimmunoassay, was increased tenfold in inflammatory bowel disease, while immunoglobulin A synthesis per 10(6) cells was unchanged. "Null" or K-lymphocytes were absent from all populations, and antibody-dependent cellular cytotoxicity (a K-cell-mediated function) was not demonstrable. Taken together, the results fail to support a role for antibody-dependent cellular cytotoxicity or a defect in secretory immunoglobulin A, but rather focus attention upon possible forms of immunoglobulin G-mediated tissue damage in the pathogenesis or perpetuation of inflammatory bowel disease.
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PMID:Characteristics of isolated intestinal mucosal lymphoid cells in inflammatory bowel disease. 31 52

Viable suspensions of human colonic mucosal lymphoid cells have been prepared by sequential treatment of tissue with dithiothreitol, EDTA in calcium- and magnesium-free salt solutions, and purified collagenase. The intestinal lymphocyte population, in comparison with that of peripheral blood, had greater numbers of bone marrow-derived cells, particularly cells bearing membrane IgA; showed spontaneous association with macrophages; underwent rapid rosette formation with sheep erythrocytes; and demonstrated increased in vitro synthesis of immunoglobulin. Total thymus-derived cells were equal in the two populations. Decreases were found in "null" cell numbers, in cells bearing membrane IgD and IgM, and in responsiveness to phytohemagglutinin. Macrophage/monocytes in the intestinal population were increased in size, granularity, motility, sustained glass adherence, and phagocytic activity. Human intestinal lymphoid cells appear to constitute a cell population that is more "mature" and/or "activated", in comparison with the lymphoid cells of peripheral blood. The method of preparation should lend itself to the study of inflammatory bowel disease, gastrointestinal cancer, and the intestinal secretory immune system.
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PMID:Isolation and functional characterization of human intestinal mucosal lymphoid cells. 32 91

The gastrointestinal tract is replete with immunocompetent tissue represented by appendix, Peyer's patches and nonaggregated lymphocytes in the intestinal epithelium. This local immune system plays a vital role in the physiologic immune response and in the control of food, drug, microbial or viral antigens. Under certain situations this lymphoid tissue may contribute to the immunological reactions underlying the pathogenesis of various diseases. Generalised deficiencies of the immune apparatus frequently give rise to disturbances of gastrointestinal function. Furthermore plenty of immune reactions occurring in connection with human inflammatory bowel disease have been described. Some immunologic features are reported as typical for a disease, the majority seems to indicate only nonspecific autoimmune reactions. The relevance of immunological mechanisms for the pathogenesis of these diseases is still not full evaluated.
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PMID:[Immunological aspects of inflammatory bowel diseases (author's transl)]. 41 89

Giardia lamblia infestation can cause severe diarrhea and malabsorption, and the diagnosis is usually made by identification of cysts in the feces, but small intestinal biopsy or smears may be required. A wide spectrum of roentgen changes may be seen. In patients with a normal immune status, the small bowel is normal or shows an inflammatory bowel disease pattern. Eradication of the parasite reverses these changes. In some patients with IgA deficiency, nodular lymphoid hyperplasia occurs, and this is usually not reversible. Other patients with hypogammaglobulinemia or dysgammaglobulinemia and giardiasis may show a sprue pattern. This pattern most often persists after eradication of the parasite. Although the triad of giardiasis, IgA deficiency, and nodular lymphoid hyperplasia has a particularly high association, these, together with diarrhea, malabsorption, and various altered immune states may occur in any combination.
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PMID:Current perspectives on giardiasis. 110 21

Six congenic lines of chickens that differ from the parental inbred line RPRL-15I5 for genes in the major histocompatibility (B) complex were used to study the influence of the B haplotypes on the response of chickens to infection with virulent infectious bursal disease virus (IBDV) at 1 day or 4 weeks of age, and on the antibody response to vaccination with live or inactivated oil-emulsion (OE) IBDV vaccines at 7 weeks of age. IBDV-induced immunodepression and lesions in the bursa, spleen, and thymus in chickens infected with virus at 1 day of age were of the same degree of severity, regardless of line of chickens used. The response of blood cells to the mitogens phytohemagglutinin-M and concanavalin A was elevated in chickens infected with IBDV at 1 day of age. In an experiment conducted to study the effect of the B haplotype on IBDV infection in 4-week-old chickens, B congenic line C-12 (B12B12) showed the highest susceptibility to clinical IBD, with mortality of 79%. No detectable difference in the serological response to vaccination with live or OE IBDV vaccines was noted among chickens of various congenic lines. We conclude that the B haplotypes may influence IBDV-induced mortality, but not immunodepression or severity of lesions in lymphoid organs, or the antibody response to live or OE IBDV vaccines.
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PMID:Response of B congenic chickens to infection with infectious bursal disease virus. 133 60

The expression of the vascular adhesion molecules ELAM-1 (endothelial leukocyte adhesion molecule 1) and VCAM-1 (vascular cell adhesion molecule 1) was evaluated in colonic mucosa of patients with inflammatory bowel disease and normal controls by immunocytochemistry. VCAM-1 was found to be constitutively expressed in lymphoid aggregates in normal colonic mucosa and was not significantly enhanced or altered in distribution in mucosa of patients with inflammatory bowel disease regardless of the activity of the inflammatory process. In contrast, ELAM-1 was not detected by these techniques in normal colonic mucosa (n = 11) or in colonic mucosa of patients with inflammatory bowel disease which was either uninvolved or quiescent (n = 30). However, high levels of ELAM-1 were consistently found on endothelial surfaces in association with active inflammation in affected areas of colonic mucosa in patients with either ulcerative colitis (n = 27) or Crohn's colitis (n = 9). In addition, ELAM-1 appeared to be present within neutrophils which had migrated into crypt abscesses in affected mucosa. Similar analysis was carried out in the cotton-top tamarin (CTT), a primate that experiences an idiopathic chronic diffuse colitis resembling human ulcerative colitis. Although anti-human VCAM-1 antibodies did not react with the CTT, anti-human ELAM-1 stained endothelial surfaces in mucosal biopsies from CTT with active colitis. No ELAM-1 was identified in mucosa of CTT in which colitis activity was quiescent. Thus ELAM-1 is expressed on colonic endothelial surfaces in association with inflammation and may play an important role in facilitating leukocyte migration into sites of active IBD involvement.
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PMID:Expression of vascular adhesion molecules in inflammatory bowel disease. 137 55

The morphologic characteristics of the colon in ulcerative colitis and Crohn's disease are well established, but specific appendiceal pathology is less clearly defined. In addition, the frequency of appendiceal involvement in children with inflammatory bowel disease has also not been delineated. We have determined the prevalence of appendiceal involvement in 41 children with inflammatory bowel disease (24 with Crohn's disease and 17 with ulcerative colitis) who required colonic resection and have defined the histopathologic characteristics of the appendix in these diseases. All appendices were abnormal. Specific changes of Crohn's disease or ulcerative colitis were observed respectively in 50% and 56% of the appendices in our patient population. Nonspecific changes only such as fibrous obliteration, serosal fibrosis and lymphoid and/or neuronal hyperplasia were noted in the remaining appendices. The severity of ileocolonic and appendiceal inflammation was similar in about two thirds of the patients with either type of inflammatory bowel disease.
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PMID:The appendix in inflammatory bowel disease in children. 149 44

The mucosal immune system is characterized predominantly by the secretory antibody response and gut-associated lymphoid tissue, cellular part of the mucosal immune system. The secretory antibody system depends on local production and selective epithelial transport of secretory IgA and IgM. Furthermore, secretory antibodies and interactions between the intestinal epithelium and T cells are involved in the mucosal down-regulation of the systemic immune system. Neuropeptides play a crucial role in the regulation of mucosal immune responses. It is possible that impairment of the mucosal immune response contributes to the pathogenesis of various intestinal diseases, such as inflammatory bowel disease. Until recently, however, mucosal immunity received relatively little attention from both basic and clinical scientists. Further research on mucosal immunity seems to have promise in helping to provide new understanding of the immune mechanisms and pathogenesis of several gastrointestinal and systemic diseases.
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PMID:Mucosal defense mechanism in health and disease. Role of the mucosal immune system. 150 99

The mucosal immune system consists of a number of compartments that are populated with a different assortment of cells and serve different functions. The cytokines produced by the cells in each of these compartments are currently being defined. This is best understood in relation to B cells, whose proliferation and maturation is guided by a sequence of cytokines. PP are inductive sites that preferentially stimulate IgA production. At least in part, this preference seems to be due to the T cells located in PP, which have been shown to stimulate switching to IgA production by cognate interactions and production of TGF-beta. Postswitch B cells expressing surface IgA respond to IL-5, a cytokine produced by T cells in GALT. Terminal differentiation to IgA-producing plasma cells in the lamina propria may be driven by IL-6, which can be produced by a variety of cells in the lamina propria and by epithelial cells. T cells in the lamina propria have an assortment of surface markers consistent with both activation and memory and appear to produce a variety of cytokines in the local environment that presumably act in normal host defense. IEL consist mainly of CD8+ T cells. They have been shown to produce IFN-gamma and, very likely, other cytokines that presumably act in a paracrine fashion on local enterocytes. How these cells and cytokines are perturbed during intestinal inflammation is currently being defined. A certain assortment of cytokines are greatly increased in IBD. This assortment, including IL-1, IL-6, and IL-8, is elevated in a wide variety of chronic inflammatory states in other tissues as well. A critical requirement for cytokines to exert their effects is the expression of specific receptors on target cells. Virtually nothing is known about this aspect of mucosal immunity, but receptor expression on mucosal cells must be defined before we will be able to understand the complex interactions among lymphoid cells, the cytokines they produce, and the local stromal and epithelial cells.
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PMID:Cells and cytokines in mucosal immunity and inflammation. 151 47


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