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Idiopathic inflammatory bowel diseases: immunological hypothesis

(1994) ACTA GASTRO-ENTEROLOGICA BELGICA. 57(5-6). p.292-299
Author
Organization
Abstract
Circumstantial evidence indicates that immunological mechanisms are important in the pathogenesis of inflammatory bower diseases, In Crohn's disease lesions the naive T cells are reduced and memory T cells are increased in number. Colonocytes of normal mucosa do not express MHC class II molecules but aberrant HLA-DR expression is induced in inflammatory conditions, Also in ileal epithelial cells there is increased MHC class II molecules expression suggesting augmented antigen presentation, Once the initiating event (environmental, dietary, infectious or enterobacterial products) has activated inflammatory cells, an autoamplifying inflammatory immunocascade is induced by numerous agents such as cytokines, transforming growth factors, leukotrienes, prostaglandins and other mediators, Tissue injury may be caused by oxygen free radicals generated by neutrophils and macrophages, The inflammatory process can be perpetuated by a persistent antigenic stimulus or alternatively, by abnormal regulation of immune and inflammatory responses, This can mean exaggerated activation of inflammatory responses to ''normal'' stimuli or defective feedback mechanisms of downregulation, The early lesions of inflammatory bower disease are patchy necrosis of the surface epithelium, focal accumulations of leukocytes adjacent to crypts and an increased number of intraepithelial lymphocytes, In Crohn's disease the earliest lesions are aphthoid ulcers overlying lymphoid follicles in the terminal ileum. In patients with spondylarthropathy and asymptomatic intestinal inflammation we demonstrated lesions in the top of the follicle associated epithelium. The changes consist of increase in number of membranous (NI) epithelial cells, ruptures, fissures and perforations of M cells, Aphthoid ulcers that may occur in the entire gastrointestinal tract are typically found at the M cell level. As NI cells are crucial in uptake and transport of antigens to the underlying lymphoid tissue, these results may indicate an immunological pathogenesis of chronic inflammatory bowel disease.
Keywords
CROHNS DISEASE, IBD, ULCERATIVE COLITIS, IMMUNOLOGY, SPONDYLARTHROPATHY, M CELLS

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Chicago
Cuvelier, Claude, Herman Mielants, Martine De Vos, and Jozef Quatacker. 1994. “Idiopathic Inflammatory Bowel Diseases: Immunological Hypothesis.” Acta Gastro-enterologica Belgica 57 (5-6): 292–299.
APA
Cuvelier, C., Mielants, H., De Vos, M., & Quatacker, J. (1994). Idiopathic inflammatory bowel diseases: immunological hypothesis. ACTA GASTRO-ENTEROLOGICA BELGICA, 57(5-6), 292–299.
Vancouver
1.
Cuvelier C, Mielants H, De Vos M, Quatacker J. Idiopathic inflammatory bowel diseases: immunological hypothesis. ACTA GASTRO-ENTEROLOGICA BELGICA. 1994;57(5-6):292–9.
MLA
Cuvelier, Claude, Herman Mielants, Martine De Vos, et al. “Idiopathic Inflammatory Bowel Diseases: Immunological Hypothesis.” ACTA GASTRO-ENTEROLOGICA BELGICA 57.5-6 (1994): 292–299. Print.
@article{194455,
  abstract     = {Circumstantial evidence indicates that immunological mechanisms are important in the pathogenesis of inflammatory bower diseases, In Crohn's disease lesions the naive T cells are reduced and memory T cells are increased in number. Colonocytes of normal mucosa do not express MHC class II molecules but aberrant HLA-DR expression is induced in inflammatory conditions, Also in ileal epithelial cells there is increased MHC class II molecules expression suggesting augmented antigen presentation, Once the initiating event (environmental, dietary, infectious or enterobacterial products) has activated inflammatory cells, an autoamplifying inflammatory immunocascade is induced by numerous agents such as cytokines, transforming growth factors, leukotrienes, prostaglandins and other mediators, Tissue injury may be caused by oxygen free radicals generated by neutrophils and macrophages, The inflammatory process can be perpetuated by a persistent antigenic stimulus or alternatively, by abnormal regulation of immune and inflammatory responses, This can mean exaggerated activation of inflammatory responses to ''normal'' stimuli or defective feedback mechanisms of downregulation, The early lesions of inflammatory bower disease are patchy necrosis of the surface epithelium, focal accumulations of leukocytes adjacent to crypts and an increased number of intraepithelial lymphocytes, In Crohn's disease the earliest lesions are aphthoid ulcers overlying lymphoid follicles in the terminal ileum. In patients with spondylarthropathy and asymptomatic intestinal inflammation we demonstrated lesions in the top of the follicle associated epithelium. The changes consist of increase in number of membranous (NI) epithelial cells, ruptures, fissures and perforations of M cells, Aphthoid ulcers that may occur in the entire gastrointestinal tract are typically found at the M cell level. As NI cells are crucial in uptake and transport of antigens to the underlying lymphoid tissue, these results may indicate an immunological pathogenesis of chronic inflammatory bowel disease.},
  author       = {Cuvelier, Claude and Mielants, Herman and De Vos, Martine and Quatacker, Jozef},
  issn         = {0001-5644},
  journal      = {ACTA GASTRO-ENTEROLOGICA BELGICA},
  keyword      = {CROHNS DISEASE,IBD,ULCERATIVE COLITIS,IMMUNOLOGY,SPONDYLARTHROPATHY,M CELLS},
  language     = {eng},
  number       = {5-6},
  pages        = {292--299},
  title        = {Idiopathic inflammatory bowel diseases: immunological hypothesis},
  volume       = {57},
  year         = {1994},
}