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Animal Models and Pathogenesis of Inflammatory Bowel Disease

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Neuroendocrinology of Gastrointestinal Ulceration

Part of the book series: Hans Selye Symposia on Neuroendocrinology and Stress ((HSSN,volume 2))

Abstract

Treatment of inflammatory bowel disease (IBD) is hampered by the fact that we know very little about the underlying causes of this condition. For instance, it remains unclear whether those alterations in immunologic function (such as autosensitization to epithelial cell components)1 or in the activity or structure of the enteric nervous system (degeneration of the autonomic nerves)2 which are characteristic of IBD represent initiating factors or are simply epiphenomena. Consequently, treatment is primarily palliative or supportive. The development of new or improved therapeutic agents and procedures, in particular, would benefit from the availability of animal models on which newly developed agents which might be of value in treatment of human disease could be tested. In particular there is a need for models which are simple to produce, which are inexpensive, and in which the induced disease is sufficiently prolonged, reproducible and severe to enable such tests to be routinely performed.

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Authors
  1. Gerald P. Morris
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  2. Paul L. Beck
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  3. John L. Wallace
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  4. Margaret S. Herridge
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  5. Carlo A. Fallone
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Editors and Affiliations

  1. Harvard Medical School, Boston, Massachusetts, USA

    Sandor Szabo

  2. Irvine VA Medical Center, University of California, Long Beach, California, USA

    Sandor Szabo

  3. Center for Ulcer Research and Education, University of California, Los Angeles, California, USA

    Yvette Taché

  4. University of Manitoba, Winnipeg, Manitoba, Canada

    Gary B. Glavin

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Morris, G.P., Beck, P.L., Wallace, J.L., Herridge, M.S., Fallone, C.A. (1995). Animal Models and Pathogenesis of Inflammatory Bowel Disease. In: Szabo, S., Taché, Y., Glavin, G.B. (eds) Neuroendocrinology of Gastrointestinal Ulceration. Hans Selye Symposia on Neuroendocrinology and Stress, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1867-9_8

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