Baillière's Clinical Gastroenterology
1 Pathogenesis of Crohn's disease
References (75)
- et al.
Expression of transforming growth factors alpha and beta in colonic mucosa in inflammatory bowel disease
Gastroenterology
(1996) - et al.
Tumor necrosis factor alpha-producing cells in the intestinal mucosa of children with inflammatory bowel disease
Gastroenterology
(1994) Leukocyte-endothelial cell recognition: three (or more) steps to specificity and diversity
Cell
(1991)- et al.
Oxidative damage and transforming growth factor beta I expression in pretumoral and tumoral lesions of human intestine
Free Radical Biology and Medicine
(1997) Interleukin-1 and interleukin-1 antagonism
Blood
(1991)- et al.
Crohn's disease after in-utero measles virus exposure
Lancet
(1996) - et al.
Randomised double-blind comparison of chimeric monoclonal antibody to tumour necrosis factor alpha (cA2) versus placebo in rheumatoid arthritis
Lancet
(1994) - et al.
CD4+ cell oligoclonality in Crohn's disease: evidence for an antigen-specific response
Human Immunology
(1996) - et al.
Mucosal subclass distribution of immunoglobulin Gproducing cells is different in ulcerative colitis and Crohn's disease of the colon
Gastroenterology
(1987) - et al.
Expression of vascular adhesion molecules in inflammatory bowel disease
Gastroenterology
(1992)
IL-10 deficient mice develop chronic enteroclitis
Cell
In vivo profiles of eicosanoids in ulcerative colitis, Crohn's colitis, and Clostridium difficile colitis
Gastroenterology
Protective effect of epidermal growth factor in an experimental model of colitis in rats
Gastroenterology
Expanded CD4+CD45RO+ phenotype and defective proliferative response in T lymphocytes from patients with Crohn's disease
Gastroenterology
Ulcerative colitis-like disease in mice with a disrupted intefieukin-2 gene
Cell
Indium-111-granulocyte scanning in the assessment of disease extent and disease activity in inflammatory bowel disease
Lysozyme gene expression in inflammatory bowel disease
Gastroenterology
Reciprocal IFN-gamma and IGF-beta responses regulate the occurrence of mucosal inflammation
Immunology Today
Granulomatous vasculitis in Crohn's disease
Gastroenterology
Crohn's disease: pathogenesis and persistent measles virus infection
Gastroenterology
Localisation of intestinal interleukin 1 activity and protein and gene expression to lamina propria cells
Gastroenterology
Lactoferrin: a correlate of disease activity in inflammatory bowel disease
European Journal of Gastroenterology and Hepatology
Faecal elastase reflects disease activity in active ulcerative colitis
Scandinavian Journal of Gastroenterology
Circulating human leucocyte elastase in patients with inflammatory bowel disease
Gut
Effect of an enteric-coated fish-oil preparation on relapses in Crohn's disease
New England Journal of Medicine
Differences in the intrinsic capacity of peripheral blood mononuclear cells to produce tumour necrosis factor alpha and beta in patients with inflammatory bowel disease and healthy controls
Scandinavian Journal of Gastroenterology
Keratinocyte growth factor is highly over-expressed in inflammatory bowel disease
American Journal of Pathology
Immunopathology of Crohn's disease
Annals of Gastroenterology and Hepatology, Paris
Paratuberculosis
Clinical Microbiological Review
Picotamide inhibition of excess in vitro thromboxane B2 release by colorectal mucosa in inflammatory bowel disease
Alimentary Pharmacology and Therapeutics
Interleukin-1 (IL-I) gene expression, synthesis, and effect of specific IL-1 receptor blockade in rabbit immune complex colitis
Journal of Clinical Investigation
Specific mucosal imbalance of IL-1 and IL-1 receptor antagonist (IL-1ra) in IBD: a potential mechanism of chronic inflammation
Gastroenterology
Bacteria-specific T cell clones are selective in their reactivity towards different enterobacteria or H. pylori and increased in inflammatory bowel disease
Scandinavian Journal of Immunology
Neutrophil cytoplasmic antibodies: a link between primary sclerosing cholangitis and ulcerative colitis
Gastroenterology
Treatment of Crohn's disease with anti- tumour necrosis factor chimeric monoclonal antibody (cA2)
Gastroenterology
Phase II trial of copper zinc superoxide dismutase (CuZn SOD) in the treatment of Crohn's disease
Free Radical Research Communications
Inducible nitric oxide synthetase (iNOS) and cyclooxygenase (COX-2) expression in ulcerative colitis and Crohn's disease
Gastroenterology
Cited by (20)
Cytokines and therapy in COPD: A promising combination?
2002, ChestCitation Excerpt :Studies in vivo in mice and humans have revealed that TNF-α is involved in the recruitment of macrophages to sites of inflammation. Thus, in chronic colitis (Crohn's disease) and rheumatoid arthritis, diseases characterized by the presence of macrophages, T cells, and neutrophils,62,63 therapy with neutralizing antibodies directed against TNF-α reduces the inflammation, whereas clinically the patients improved, showing reduced symptoms and an improved quality of life.64,65,66,67,68 In addition, in Crohn's disease, > 30% of the fistulae closed.67
Detection of Mycobacterium avium subspecies paratuberculosis in Crohn's diseased tissues by in situ hybridization
2001, American Journal of GastroenterologyCitation Excerpt :Although controversial, further support of the mycobacterial etiology in CD disease are: 1) the recent emergence of cell wall-deficient (CWD) forms of M. paratuberculosis in cultures from tissue specimens and milk of a portion of the patients with CD (7–13), 2) the high frequency in detecting M. paratuberculosis DNA in CD tissues (14–18), 3) the successful therapy of CD patients with antimycobacterial treatment containing macrolide antibiotics (19–21), and 4) the specific seroreactivity of the majority of CD patient serum samples specifically against M. paratuberculosis antigens (22–24). The variation of disease severity, relapses, and remissions, and response to treatment between individual patients, however, makes these results inconsistent among all investigators and creates controversy about an etiology of this disease (25–27). Hence, it is tempting to believe of CD as a group of disorders, of different etiologies, but with similar presentation and that one of these disorders is triggered or caused by M. paratuberculosis, specifically its CWD form.
Etiology of Crohn's disease: The role of Mycobacterium avium paratuberculosis
2001, Trends in Molecular MedicineEstablished and emerging biological activity markers of inflammatory bowel disease
2000, American Journal of GastroenterologyCitation Excerpt :In CD, the presence of abscesses may lead to elevated PMN counts, while complicating lymphangiectasia results in lymphocyte loss through the intestinal wall, and thus a reduced number of circulating T cells (15). In some UC patients a distinct leukocytosis occurs, which, at the tissue level, may be associated with the healing phase (16). However, in general, this marker is not useful for assessment of IBD activity in clinical practice.
Neutropenia, neutrophil dysfunction, and inflammatory bowel disease in glycogen storage disease type Ib: Results of the European study on glycogen storage disease type I
2000, Journal of PediatricsCitation Excerpt :The IBD in GSD-Ib resembles Crohn's disease and may involve the entire gastrointestinal tract. In the absence of a single etiologic factor, Crohn's disease can be regarded as a manifestation of poorly regulated immune and inflammatory processes within the gut wall.28 In most cases of Crohn's disease, neutrophils probably contribute to the tissue damage.29
New emerging and re-emerging bacterial foodborne pathogens
2012, Kafkas Universitesi Veteriner Fakultesi Dergisi