TY - JOUR

T1 - Mediators of inflammation in chronic inflammatory bowel disease

AU - Nielsen, O. H.

AU - Rask-Madsen, J.

PY - 1996/4/22

Y1 - 1996/4/22

N2 - A distinguishing feature of inflammatory bowel disease (IBD) is its apparently spontaneous, chronic relapsing course. Despite extensive research over several decades the etiology of IBD remains unknown, but evidence has accumulated to suggest that the mucosal inflammatory response may be caused by (i) a defective mucosal barrier function resulting in an abnormally increased exposure to luminal antigens and toxins, (ii) an appropriate immunologic response to an unusual infection, antigen or toxin, or (iii) an inappropriate immunological response to ubiquitous antigens or stimuli. In recent years, the identification of established and potential mediators of inflammation has expanded to include eicosanoids, platelet activating factor, biogenic amines, kinins, complement-derived peptides, chemotactic peptides, cytokines, neuropeptides, and reactive metabolites of oxygen and nitrogen. Thus, the study of the inflammatory process has become ever more complex. Until the predisposing and trigger factors have been identified the achievement of a more rational and effective approach to therapy in IBD relies on interruption of the mechanisms responsible for excess mediator formation. As summarized in this review on the role of soluble mediators of inflammation, several Danish gastroenterologists have been profoundly engaged in basic and clinical research in the past 25 years to place some pieces of the confusing puzzle of IBD.

AB - A distinguishing feature of inflammatory bowel disease (IBD) is its apparently spontaneous, chronic relapsing course. Despite extensive research over several decades the etiology of IBD remains unknown, but evidence has accumulated to suggest that the mucosal inflammatory response may be caused by (i) a defective mucosal barrier function resulting in an abnormally increased exposure to luminal antigens and toxins, (ii) an appropriate immunologic response to an unusual infection, antigen or toxin, or (iii) an inappropriate immunological response to ubiquitous antigens or stimuli. In recent years, the identification of established and potential mediators of inflammation has expanded to include eicosanoids, platelet activating factor, biogenic amines, kinins, complement-derived peptides, chemotactic peptides, cytokines, neuropeptides, and reactive metabolites of oxygen and nitrogen. Thus, the study of the inflammatory process has become ever more complex. Until the predisposing and trigger factors have been identified the achievement of a more rational and effective approach to therapy in IBD relies on interruption of the mechanisms responsible for excess mediator formation. As summarized in this review on the role of soluble mediators of inflammation, several Danish gastroenterologists have been profoundly engaged in basic and clinical research in the past 25 years to place some pieces of the confusing puzzle of IBD.

KW - Chemotactic factors

KW - Colitis, ulcerative

KW - Complement

KW - Crohn disease

KW - Cytokines

KW - Eicosanoids

KW - Inflammatory bowel disese

KW - Inflammatory mediators

KW - Leukotrienes

KW - Neuropeptides

KW - Nitric oxide

KW - Platelet activating factor

KW - Prostaglandins

KW - Reactive oxygen species

UR - http://www.scopus.com/inward/record.url?scp=0029932723&partnerID=8YFLogxK

M3 - Review

C2 - 8726287

AN - SCOPUS:0029932723

VL - 31

SP - 149

EP - 159

JO - Scandinavian Journal of Gastroenterology

JF - Scandinavian Journal of Gastroenterology

SN - 0036-5521

IS - 216

ER -