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Ulcerative colitis and indeterminate colitis in a defined populationStewénius, Jan. January 1995 (has links)
Thesis (doctoral)--Lunds universitet, 1995. / Added t.p. with thesis statement inserted.
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Ulcerative colitis and indeterminate colitis in a defined populationStewénius, Jan. January 1995 (has links)
Thesis (doctoral)--Lunds universitet, 1995. / Added t.p. with thesis statement inserted.
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Ulcerative and experimental colitis pathophysiology as basis for therapeutic intervention /Fabia, Renata. January 1993 (has links)
Thesis (doctoral)--Lund University, 1993. / Added t.p. with thesis statement inserted.
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Ulcerative and experimental colitis pathophysiology as basis for therapeutic intervention /Fabia, Renata. January 1993 (has links)
Thesis (doctoral)--Lund University, 1993. / Added t.p. with thesis statement inserted.
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Protein synthesis and gastrointestinal pathophysiology in a piglet model of colitis importance of nutrition and probiotics /Harding, Scott V. January 1900 (has links)
Thesis (Ph.D.). / Written for the School of Dietetics and Human Nutrition. Title from title page of PDF (viewed 2007/08/29). Includes bibliographical references.
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The role of co-stimulatory molecules and inflammatory cytokines in a murine model of inflammatory bowel diseaseSingh, Baljit January 2003 (has links)
No description available.
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Appendicitis protects against colitis: an exploration of underlying immune mechanismsNg, Wa Sang Watson, Medical Sciences, Faculty of Medicine, UNSW January 2008 (has links)
Inflammatory bowel disease-(IBD) is a chronic relapsing and remitting disorder of the gastrointestinal tract characterised by inflammation. The underlying immunopathogenesis is unknown but excessive effector and defective regulatory immune responses play a significant role. The aetiology of IBD is not yet fully resolved, but interactions between genetic and environmental factors, including the gut flora, contribute significantly to the development of IBD. Appendicectomy for intra-abdominal inflammatory conditions before the age of 20 protects against colitis. The mechanism underlying this protective effect is unclear. This thesis examined the hypothesis that appendiceal regulatory T lymphocytes (Treg) mediate the protection. Despite human and murine data showing that the appendix is involved in the prevention of colitis, few studies of human or murine appendices have been reported. A novel murine model of appendicitis was created using an operative technique of band-ligation of an induced-tubular-appendix. Histological assessment showed that this model recapitulated all of the histological features of human acute appendicitis, namely mucosal ulceration, transmural neutrophilic and lymphocytic infiltration and serositis. This local pathology was associated with a systemic host response, evidenced by raised serum Creactive- protein. The impact of inflammation on the appendiceal lymphocyte constituents was assessed by flow cytometry. The inflammation caused a shift from B-lymphocyte to T-lymphocyte predominance. In particular there was a 75% increment in Treg numbers, which was restricted to juvenile mice only (< 10 weeks old). Furthermore, appendiceal Treg expressed the gut-homing chemokine-receptor, CCR9, and the intestine-specific integrin, α4β7. These cells were shown to preferentially migrate to the colonic lamina propria. Lastly, appendicitis and appendicectomy protected against TNBS-colitis which was also restricted to juvenile mice. Evidence for antigen dependence was suggested by the effect being heightened when mice were pre-sensitised against TNBS. Exploration of the colonic lamina propria (cLP) lymphocyte population showed an increase in Treg, especially CD8+Foxp3+- Treg, in ??protected?? mice only, which may have originated in the appendix. Intracytoplasmic cytokine detection showed that these cLP-Treg were potent producers of the regulatory cytokine, IL-10. These findings strongly suggest that appendicitis triggers an expansion of Treg which then emigrate to the colon and mediate long-lasting protection against colitis.
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Appendicitis protects against colitis: an exploration of underlying immune mechanismsNg, Wa Sang Watson, Medical Sciences, Faculty of Medicine, UNSW January 2008 (has links)
Inflammatory bowel disease-(IBD) is a chronic relapsing and remitting disorder of the gastrointestinal tract characterised by inflammation. The underlying immunopathogenesis is unknown but excessive effector and defective regulatory immune responses play a significant role. The aetiology of IBD is not yet fully resolved, but interactions between genetic and environmental factors, including the gut flora, contribute significantly to the development of IBD. Appendicectomy for intra-abdominal inflammatory conditions before the age of 20 protects against colitis. The mechanism underlying this protective effect is unclear. This thesis examined the hypothesis that appendiceal regulatory T lymphocytes (Treg) mediate the protection. Despite human and murine data showing that the appendix is involved in the prevention of colitis, few studies of human or murine appendices have been reported. A novel murine model of appendicitis was created using an operative technique of band-ligation of an induced-tubular-appendix. Histological assessment showed that this model recapitulated all of the histological features of human acute appendicitis, namely mucosal ulceration, transmural neutrophilic and lymphocytic infiltration and serositis. This local pathology was associated with a systemic host response, evidenced by raised serum Creactive- protein. The impact of inflammation on the appendiceal lymphocyte constituents was assessed by flow cytometry. The inflammation caused a shift from B-lymphocyte to T-lymphocyte predominance. In particular there was a 75% increment in Treg numbers, which was restricted to juvenile mice only (< 10 weeks old). Furthermore, appendiceal Treg expressed the gut-homing chemokine-receptor, CCR9, and the intestine-specific integrin, α4β7. These cells were shown to preferentially migrate to the colonic lamina propria. Lastly, appendicitis and appendicectomy protected against TNBS-colitis which was also restricted to juvenile mice. Evidence for antigen dependence was suggested by the effect being heightened when mice were pre-sensitised against TNBS. Exploration of the colonic lamina propria (cLP) lymphocyte population showed an increase in Treg, especially CD8+Foxp3+- Treg, in ??protected?? mice only, which may have originated in the appendix. Intracytoplasmic cytokine detection showed that these cLP-Treg were potent producers of the regulatory cytokine, IL-10. These findings strongly suggest that appendicitis triggers an expansion of Treg which then emigrate to the colon and mediate long-lasting protection against colitis.
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Appendicitis protects against colitis: an exploration of underlying immune mechanismsNg, Wa Sang Watson, Medical Sciences, Faculty of Medicine, UNSW January 2008 (has links)
Inflammatory bowel disease-(IBD) is a chronic relapsing and remitting disorder of the gastrointestinal tract characterised by inflammation. The underlying immunopathogenesis is unknown but excessive effector and defective regulatory immune responses play a significant role. The aetiology of IBD is not yet fully resolved, but interactions between genetic and environmental factors, including the gut flora, contribute significantly to the development of IBD. Appendicectomy for intra-abdominal inflammatory conditions before the age of 20 protects against colitis. The mechanism underlying this protective effect is unclear. This thesis examined the hypothesis that appendiceal regulatory T lymphocytes (Treg) mediate the protection. Despite human and murine data showing that the appendix is involved in the prevention of colitis, few studies of human or murine appendices have been reported. A novel murine model of appendicitis was created using an operative technique of band-ligation of an induced-tubular-appendix. Histological assessment showed that this model recapitulated all of the histological features of human acute appendicitis, namely mucosal ulceration, transmural neutrophilic and lymphocytic infiltration and serositis. This local pathology was associated with a systemic host response, evidenced by raised serum Creactive- protein. The impact of inflammation on the appendiceal lymphocyte constituents was assessed by flow cytometry. The inflammation caused a shift from B-lymphocyte to T-lymphocyte predominance. In particular there was a 75% increment in Treg numbers, which was restricted to juvenile mice only (< 10 weeks old). Furthermore, appendiceal Treg expressed the gut-homing chemokine-receptor, CCR9, and the intestine-specific integrin, α4β7. These cells were shown to preferentially migrate to the colonic lamina propria. Lastly, appendicitis and appendicectomy protected against TNBS-colitis which was also restricted to juvenile mice. Evidence for antigen dependence was suggested by the effect being heightened when mice were pre-sensitised against TNBS. Exploration of the colonic lamina propria (cLP) lymphocyte population showed an increase in Treg, especially CD8+Foxp3+- Treg, in ??protected?? mice only, which may have originated in the appendix. Intracytoplasmic cytokine detection showed that these cLP-Treg were potent producers of the regulatory cytokine, IL-10. These findings strongly suggest that appendicitis triggers an expansion of Treg which then emigrate to the colon and mediate long-lasting protection against colitis.
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Pathogenesis of immune-mediated murine colitisJong, Ype Peter de. January 2002 (has links)
Proefschrift Universiteit van Amsterdam. / Met bibliogr., lit. opg. - Met samenvatting in het Nederlands.
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