A primary dysregulation in the immunoregulatory role of the intestinal mucosal epithelial cell in inflammatory bowel disease pathogenesis? Biology of inflammatory response as tissue pattern entities in Crohn's versus ulcerative colitis

被引:7
作者
Agius, LM [1 ]
机构
[1] Univ Malta, Sch Med, St Lukes Hosp, Dept Pathol, Msida, Malta
关键词
immunoregulation; inflammatory bowel disease; pattern response; epithelial cell;
D O I
10.1016/j.jtbi.2003.11.002
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Within a framework of dual involvement of mucosa and submucosa on the one hand, and of the muscularis propria of the bowel wall on the other, it might be valid to consider involvement of the vascular supply as the essential means in itself of not only causing the morphologic lesions in inflammatory bowel disease, but also especially in accounting for persisting patterns of inflammatory response both in ulcerative colitis and in Crohn's disease. Inflammatory bowel disease as a group constitutes a spectrum of biologic and pathobiologic manifestations in terms not only of inflammatory involvement of the bowel wall but also in terms of how the bowel in its turn deals with inflammation as a pathologic lesion in its own right. Parameters of inflammatory bowel activity transcend simple concepts of etiology and pathogenesis as applicable to category disorders such as infections or bowel ischemia. Indeed, the strictly characterized initiation of the inflammatory bowel response as a function of defective regulation of the antigenicity of the luminal contents on the one hand, and on interactions between nitric oxide and free oxygen radicals on the other, might help determine a persistence of tissue damage in inflammatory bowel disease that is either relapsing/remitting or chronic in progression. In a final analysis, perhaps, there might be involved a single central form of pathway induction of dysregulated immune reactivity arising from an early disturbance in activation patterns as induced by the onset of luminal antigenicity at an early or specific-stage, further characterized perhaps by specific forms of intestinal epithelial defects of the bowel mucosa in patients subsequently developing inflammatory bowel disease. Specific genetic markers for disease susceptibility and for therapeutic responsiveness are particularly of interest. The Nucleotide binding oligomerization Domain 2 (NOD2) would recognize microbial lipopolysaccharide or else mark systemic responses to pathogens that are pathogenic to evolving inflammatory bowel disease. (C) 2003 Elsevier Ltd. All rights reserved.
引用
收藏
页码:219 / 228
页数:10
相关论文
共 63 条
[11]   Low grade dysplasia in extensive, long-standing inflammatory bowel disease - A follow-up study [J].
Befrits, R ;
Ljung, T ;
Jaramillo, E ;
Rubio, C .
DISEASES OF THE COLON & RECTUM, 2002, 45 (05) :615-620
[12]   Perturbative quantum gravity and its relation to gauge theory [J].
Bern Z. .
Living Reviews in Relativity, 2002, 5 (1)
[13]   Resident bacterial flora and immune system [J].
Biancone, L ;
Monteleone, I ;
Blanco, GD ;
Vavassori, P ;
Pallone, F .
DIGESTIVE AND LIVER DISEASE, 2002, 34 :S37-S43
[14]   The immunological and genetic basis of inflammatory bowel disease [J].
Bouma, G ;
Strober, W .
NATURE REVIEWS IMMUNOLOGY, 2003, 3 (07) :521-533
[15]   Defining complex contributions of NOD2/CARD15 gene mutations, age at onset, and tobacco use on Crohn's disease phenotypes [J].
Brant, SR ;
Picco, MF ;
Achkar, JP ;
Bayless, TM ;
Kane, SV ;
Brzezinski, A ;
Nouvet, FJ ;
Bonen, D ;
Karban, A ;
Dassopoulos, T ;
Karaliukas, R ;
Beaty, TH ;
Hanauer, SB ;
Duerr, RH ;
Cho, JH .
INFLAMMATORY BOWEL DISEASES, 2003, 9 (05) :281-289
[16]   Tumor necrosis factor antagonist therapy and lymphoma development - Twenty-six cases reported to the Food and Drug Administration [J].
Brown, SL ;
Greene, MH ;
Gershon, SK ;
Edwards, ET ;
Braun, MM .
ARTHRITIS AND RHEUMATISM, 2002, 46 (12) :3151-3158
[17]   Role of enteric glial cells in inflammatory bowel disease [J].
Cabarrocas, J ;
Savidge, TC ;
Liblau, RS .
GLIA, 2003, 41 (01) :81-93
[18]   Serological differentiation of inflammatory bowel diseases [J].
Conrad, K ;
Schmechta, H ;
Klafki, A ;
Lobeck, G ;
Uhlig, HH ;
Gerdi, S ;
Henker, J .
EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY, 2002, 14 (02) :129-135
[19]   Effects of appendicectomy on the course of ulcerative colitis [J].
Cosnes, J ;
Carbonnel, F ;
Beaugerie, L ;
Blain, A ;
Reijasse, D ;
Gendre, JP .
GUT, 2002, 51 (06) :803-807
[20]   Factors regulating the effect of IL-4 on intestinal epithelial barrier function [J].
Di Leo, V ;
Yang, PC ;
Berin, MC ;
Perdue, MH .
INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, 2002, 129 (03) :219-227