Role of Appendicitis and Appendectomy in the Pathogenesis of Ulcerative Colitis: A Critical Review

Koutroubakis, Ioannis E.; Vlachonikolis, Ioannis G.; Kouroumalis, Elias

doi:10.1097/00054725-200207000-00007

Cited by 134 publications

(68 citation statements)

References 73 publications

(109 reference statements)

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“…For instance, a meta-analysis evaluating 13 case-control studies, and the combined results of the individual studies suggest that removal of the appendix reduces the risk of developing ulcerative colitis by 69% [4]. Appendectomy in the dextran sodium sulfate mouse model, and T cell receptor-·-deficient mouse model of colitis, protects animals from establishing severe inflammatory disease [10,11].…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, appendectomy is protective for patients against the development of ulcerative colitis, and has been reported to reduce the risk of acquiring intestinal disease [4][5][6]. Moreover, a Swedish meta-analysis by Andersson [7] has demonstrated a negative association between appendectomy and ulcerative colitis, as well as Crohn's disease.…”

Section: Introductionmentioning

confidence: 99%

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Preferential Migration of CD62L<sup>+</sup> Cells into the Appendix in Mice with Experimental Chronic Colitis

Farkas¹,

Hornung²,

Sattler³

et al. 2005

Eur Surg Res

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Background: Clinical and experimental studies suggest that appendectomy can protect against development of ulcerative colitis and Crohn’s disease. However, how T cells in the appendix affect the development of colitis has not been clarified. Aim: To investigate the in vivo migration and activation of colitis-inducing CD62L⁺ cells during development of chronic colitis. Methods: CD62L⁺CD4⁺ cells were fluorescently labeled and transferred to severe combined immunodeficient (SCID) mice to induce colitis. In vivo migration of T cells into the mucosa of the appendix and colon was quantified by in vivo microscopy after 7 weeks. In a second experiment, unlabeled CD62L⁺CD4⁺ cells were transferred, reisolated after 7 weeks, and adhesion molecule (integrin α₄β₇) and costimulatory molecule (CD154) expression was analyzed. Results: Six to eight weeks after CD62L⁺CD4⁺ cell transfer, SCID mice developed chronic colitis. In vivo microscopic analysis demonstrated a preferential migration of fluorescence-labeled CD62L⁺CD4⁺cells into the mucosa of the appendix versus the colon. Re-isolation of lamina propria cells from mice with colitis confirmed that CD62L⁺CD4⁺ cell migration was significantly enhanced in the appendix, compared to the colon (3.5-fold). Furthermore, a higher proportion of CD62L⁺CD4⁺ cells re-isolated from the appendix expressed integrin α₄β₇ and CD154 than from the colon. Conclusion: This study demonstrates the preferential migration of CD62L⁺CD4⁺cells into the appendix as compared to the colon. This migration pattern correlated with upregulation of integrin α₄β₇and CD154 (CD40 ligand) on T cells. Our results suggest an important role of the appendix in the pathogenesis of colitis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Preferential Migration of CD62L<sup>+</sup> Cells into the Appendix in Mice with Experimental Chronic Colitis

Farkas¹,

Hornung²,

Sattler³

et al. 2005

Eur Surg Res

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“…Findings from a registry-based study in Sweden indicate that it is appendicitis, and not the appendicectomy as such, that is associated with a decreased risk of UC, giving further credence to such a hypothesis [97] . In addition, in a meta-analysis [98] from 2002, a pooled protective effect was reported for an appendectomy in UC in 17 case-control studies with an OR of 0.31 (95% CI 0.26-0.37). All these studies have suggested that alterations in mucosal immune responses leading to appendicitis or resulting from appendectomy may negatively affect the pathogenetic mechanisms of UC.…”

Section: Appendectomymentioning

confidence: 99%

Environmental Factors Affecting Inflammatory Bowel Disease: Have We Made Progress?

Lakatos

2009

Dig Dis

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The pathogenesis of inflammatory bowel disease (IBD) is only partially understood; various environmental and host (e.g. genetic, epithelial, immune, and nonimmune) factors are involved. The critical role for environmental factors is strongly supported by recent worldwide trends in IBD epidemiology. One important environmental factor is smoking. A meta-analysis partially confirms previous findings that smoking was found to be protective against ulcerative colitis and, after the onset of the disease, might improve its course, decreasing the need for colectomy. In contrast, smoking increases the risk of developing Crohn’s disease and aggravates its course. The history of IBD is dotted by cyclic reports on the isolation of specific infectious agents responsible for Crohn’s disease or ulcerative colitis. The more recently published cold chain hypothesis is providing an even broader platform by linking dietary factors and microbial agents. An additional, recent theory has suggested a breakdown in the balance between putative species of ‘protective’ versus ‘harmful’ intestinal bacteria – this concept has been termed dysbiosis resulting in decreased bacterial diversity. Other factors such as oral contraceptive use, appendectomy, dietary factors (e.g. refined sugar, fat, and fast food), perinatal events, and childhood infections have also been associated with both diseases, but their role is more controversial. Nonetheless, there is no doubt that economic development, leading to improved hygiene and other changes in lifestyle (‘westernized lifestyle’) may play a role in the increase in IBD. This review article focuses on the role of environmental factors in the pathogenesis and progression of IBDs.

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“…28 Other environmental risk factors In observational studies, appendectomies appear to provide a risk reduction in the development of UC. 29 Oral contraceptives statistically significantly increased the risk for developing CD and appeared to increase the risk of UC. 30 The other important environmental factor playing on the development of IBD is diet control.…”

Section: Introductionmentioning

confidence: 96%

Inflammatory bowel disease and oral health

Chandan

Thomas

2017

BDJ Team

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Risk factors involved in IBDIBD is thought to result from inappropriate and ongoing activation of the mucosal immune system facilitated by defects in both the intestinal epithelium and mucosal immune system. 5 There are both genetic and environmental factors implicated in the aetiology of IBD. 6 Although traditionally associated with the developed world, recent epidemiological studies suggest an increasing incidence in rapidly developing countries, especially in South-East Asia. 7 In addition, the increased risk of IBD in the immigrant populations in the West suggests environment has a role in the development of IBD. 8 Genetic Detailed genetic mapping has identified specific genetic changes on chromosome 16 carried in families which appear linked to CD, however no significant changes have been mapped as of yet to UC. 9,10 Specifically, variants of the NOD2 gene provide the strongest association with susceptibility to CD. NOD2 plays a key role in regulating the gut mucosal barrier involving, specifically, the microbiota, as well as the related response by the innate and adaptive immune system. The IBDchip European Project showed NOD2 has been implicated in ileal location colitis with stenosing and penetrating disease behaviour. 11 A genome wide association study has also identified a strong link between the IL23R gene and CD. 12 The gene in particular codes for interleukin 23 that plays a role in regulating innate immunity within the intestine. 13 Cigarette smoking Unusually, cigarette smoking is associated with decreased rates of incidence of UC and has been associated with protective features to prevent further flare-ups of the condition 14-19 such as relapses, 20 ©SEBASTIAN KAULITZKI/Science Photo Library/Getty J. S. Chandan 1 and T. Thomas 1 summarise the treatments for inflammatory bowel disease (IBD) and how anti-inflammatory medications can have side effects that affect the oral cavity.

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Role of Appendicitis and Appendectomy in the Pathogenesis of Ulcerative Colitis: A Critical Review

Cited by 134 publications

References 73 publications

Preferential Migration of CD62L<sup>+</sup> Cells into the Appendix in Mice with Experimental Chronic Colitis

Preferential Migration of CD62L<sup>+</sup> Cells into the Appendix in Mice with Experimental Chronic Colitis

Environmental Factors Affecting Inflammatory Bowel Disease: Have We Made Progress?

Inflammatory bowel disease and oral health

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