Guidelines for the initial biopsy diagnosis of suspected chronic idiopathic inflammatory bowel disease. The British Society of Gastroenterology Initiative.

Jenkins, David; Balsitis, M; Gallivan, S; Dixon, M. F.; Gilmour, H M; Shepherd, Neil A.; Theodossi, A; Williams, Geraint T.

doi:10.1136/jcp.50.2.93

Cited by 331 publications

(274 citation statements)

References 70 publications

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“…did a conventional histological assessment on formalin-fixed rectal and sigmoid biopsy tissue from each subject using hematoxylin and eosin-stained sections and standardized, published criteria (22).…”

Section: Histological Assessment Of Sigmoid and Rectal Biopsiesmentioning

confidence: 99%

Alterations in Expression of p11 and SERT in Mucosal Biopsy Specimens of Patients With Irritable Bowel Syndrome

et al. 2007

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Background/Aim-The pathophysiology of irritable bowel syndrome (IBS) remains enigmatic; abnormalities in serotonin metabolism have been implicated. Two proteins that influence the function of serotonin and serotonergic receptors are serotonin transporter protein (SERT or soluble carrier protein SLC6A4) and p11 (S-100A10, or calpactin I light chain). Both proteins are reported to be associated with depression-like states, a frequent co-morbid condition in IBS. We explored the hypothesis that expression of these two proteins in colonic and rectal mucosa is abnormal in patients with IBS as compared to healthy controls.

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Section: Histological Assessment Of Sigmoid and Rectal Biopsiesmentioning

confidence: 99%

Alterations in Expression of p11 and SERT in Mucosal Biopsy Specimens of Patients With Irritable Bowel Syndrome

et al. 2007

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“…Genetic predisposition, persistent infection, a defective mucosal barrier and an abnormal host immune response to food Ags may all play a role in the etiology of human IBD. Crohn's disease manifests primarily as a transmural inflammation involving the full thickness of the bowel wall that frequently leads to fissuring ulcers, fistulas, and abscess formation (29). Crohn's disease is further characterized by the presence of typical aphthous ulcers, by transmural lymphoid hyperplasia, and by the presence of granulomas.…”

Section: Figurementioning

confidence: 99%

Prevention of Experimental Colitis in SCID Mice Reconstituted with CD45RBhigh CD4+ T Cells by Blocking the CD40-CD154 Interactions

Liu¹,

Geboes

Colpaert³

et al. 2000

The Journal of Immunology

119

103

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Increased expression of CD40 and CD40 ligand (CD40L or CD154) has been found in inflamed mucosa of human inflammatory bowel disease (IBD), and interactions between these molecules seem to be involved in local cytokine production by macrophages. However, the precise role of CD40 signaling in the pathogenesis of IBD is still poorly understood. The aim of the present study was to investigate the in vivo relevance of CD40 signaling in experimental colitis in SCID mice reconstituted with syngeneic CD45RBhighCD4+ T cells. The results demonstrated that CD40+ and CD40L+ cells as well as their mRNA levels were significantly increased in inflamed mucosa. Administration of anti-CD40L neutralizing mAb over an 8-wk period starting immediately after CD45RBhighCD4+ T cell reconstitution completely prevented symptoms of wasting disease. Intestinal mucosal inflammation was effectively prevented, as revealed by abrogated leukocyte infiltration and decreased CD54 expression and strongly diminished mRNA levels of the proinflammatory cytokines IFN-γ, TNF, and IL-12. When colitic SCID mice were treated with anti-CD40L starting at 5 wk after T cell transfer up to 8 wk, this delayed treatment still led to significant clinical and histological improvement and down-regulated proinflammatory cytokine secretion. These data suggest that the CD40-CD40L interactions are essential for the Th1 inflammatory responses in the bowel in this experimental model of colitis. Blockade of CD40 signaling may be beneficial to human IBD.

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“…But these findings are well recognised as not being diagnostic of colitis. [16][17][18][19][20][21] "It should be noted that the diagnosis of colitis requires evidence of injury to the epithelium, and not simply a mild increase in the amount of chronic inflammatory infiltrate within the lamina propria," says, for example, Elizabeth Montgomery, a pathologist at Johns Hopkins University, Baltimore, in a standard textbook. 22 Bifid glands-generally considered unremarkable-are noted by Dhillon in five patients, and for only two did his observations of cell numbers find more than what he calls "slight" increases or "occasional" inflammatory cells.…”

Section: Objections Were Withdrawnmentioning

confidence: 99%

Pathology reports solve "new bowel disease" riddle

Deer¹

2011

BMJ

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Guidelines for the initial biopsy diagnosis of suspected chronic idiopathic inflammatory bowel disease. The British Society of Gastroenterology Initiative.

Cited by 331 publications

References 70 publications

Alterations in Expression of p11 and SERT in Mucosal Biopsy Specimens of Patients With Irritable Bowel Syndrome

Alterations in Expression of p11 and SERT in Mucosal Biopsy Specimens of Patients With Irritable Bowel Syndrome

Prevention of Experimental Colitis in SCID Mice Reconstituted with CD45RBhigh CD4+ T Cells by Blocking the CD40-CD154 Interactions

Pathology reports solve "new bowel disease" riddle

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