Intestinal alpha-defensin expression in pediatric inflammatory bowel disease1

Zilbauer, Matthias; Jenke, Andreas; Wenzel, G; Goedde, Daniel; Postberg, Jan; Ad, Phillips; Lucas, Mariana; Noble‐Jamieson, G.; Torrente, Franco; Salvestrini, Camilla; Heuschkel, R; Wirth, Stéfan

doi:10.1002/ibd.21577

Cited by 27 publications

(19 citation statements)

References 29 publications

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“…Recognition of MDP by NOD2 drives the activation of the pro-inflammatory transcription factor NF-jB and mitogen-activated protein kinase (MAPK) [75,78]. The importance of NOD2 in intestinal disease is supported by studies that show variants in NOD2 gene to predispose individuals to Crohn's disease [79][80][81][82][83]. NOD2 was most commonly associated with a role in immune cells such as macrophages, dendritic cells, granulocytes [78,84,85], but has also been shown to be expressed in intestinal epithelial cells [34].…”

Section: Nod2/card15mentioning

confidence: 76%

The role of innate immune-stimulated epithelial apoptosis during gastrointestinal inflammatory diseases

Siggers

Hackam

2011

Cell. Mol. Life Sci.

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The maintenance of mucosal barrier equilibrium in the intestine requires a delicate and dynamic balance between enterocyte loss by apoptosis and the generation of new cells by proliferation from stem cell precursors at the base of the intestinal crypts. When the balance shifts towards either excessive or insufficient apoptosis, a broad range of gastrointestinal diseases can manifest. Recent work from a variety of laboratories has provided evidence in support of a role for receptors of the innate immune system, including Toll-like receptors 2, 4, and 9 as well as the intracellular pathogen recognition receptor NOD2/CARD15, in the initiation of enterocyte apoptosis. The subsequent induction of enterocyte apoptosis in response to the activation of these innate immune receptors plays a key role in the development of various intestinal diseases, including necrotizing enterocolitis, Crohn's disease, ulcerative colitis, and intestinal cancer. This review will detail the regulatory pathways that govern enterocyte apoptosis, and will explore the role of the innate immune system in the induction of enterocyte apoptosis in gastrointestinal disease.

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Section: Nod2/card15mentioning

confidence: 76%

The role of innate immune-stimulated epithelial apoptosis during gastrointestinal inflammatory diseases

Siggers

Hackam

2011

Cell. Mol. Life Sci.

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“…However, these results might be influenced by serum anti-bacterial proteins (e.g. immunoglobulins and complement components) from mucosal bleeding, and by the increased secretion of antibacterial peptides such as defensins [42]. On the other hand, the effects of such factors can be omitted during the remission phase.…”

Section: Discussionmentioning

confidence: 99%

Terminal Restriction Fragment Length Polymorphism Analysis of the Gut Microbiota Profiles of Pediatric Patients with Inflammatory Bowel Disease

Aomatsu

Imaeda²,

Fujimoto³

et al. 2012

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Background/Aim: We analyzed the fecal microbiota profiles of pediatric patients with inflammatory bowel disease. Method: Terminal restriction fragment length polymorphism analysis was performed in 10 fecal samples from Crohn’s disease (CD), 14 samples from ulcerative colitis (UC) and 27 samples from healthy individuals. The bacterial diversity was evaluated by the Shannon diversity index. Result: In CD patients, a setting of similarity generated three major clusters. The majority of CD patients were classified into CD clusters I and II (9 out of 10), but the majority of healthy individuals (21 of 27) were classified into CD cluster III. In UC patients, a setting of similarity also generated three major UC clusters, but each cluster was not characteristic for UC patients or healthy individuals. The changes in simulated bacterial composition indicated that the class Clostridia, including the genus Faecalibacterium, was significantly decreased in CD patients as compared to UC patients and/or healthy individuals. The genus Bacteroides was also decreased as compared to healthy individuals. The bacterial diversity measured by the Shannon diversity index was significantly reduced in CD patients as compared to healthy individuals. Conclusion: The gut microbiota profile of pediatric CD patients was different from that of healthy children.

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“…Increased colonic Paneth cells in IBD may be part of an adaptive reaction in which alpha defensins constitute a protective barrier that helps prevent secondary mucosal infection in already inflamed bowel [22]. Alternatively, it has been suggested that PCM in the colon may exacerbate or even initiate IBD there [23]. The interplay of factors is complex and the role of Paneth cells in the pathogenesis of colonic IBD remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Paneth cell metaplasia in newly diagnosed inflammatory bowel disease in children

et al. 2014

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BackgroundPaneth cell metaplasia (PCM) is well described in adults but little is known about the distribution of colonic Paneth cells and the occurrence of PCM in a paediatric population. The aim of this study is to determine whether Paneth cell hyperplasia or metaplasia characteristically occurs in the colons of children with newly diagnosed idiopathic inflammatory bowel disease (IBD).MethodsWe retrospectively reviewed colonic series from 28 new diagnoses of paediatric IBD at a tertiary referral centre, and from a further 14 children with IBD-like symptoms whose colonic biopsies and ancillary investigations were normal. Paneth cells were counted at 6 anatomical sites in the colon, and at each site acute and chronic inflammation were assessed semi-quantitatively and the presence or absence of crypt architectural distortion and eosinophilia was documented.ResultsIn control, ulcerative colitis (UC) and Crohn’s disease (CD) groups there was a gradient of decreasing Paneth cell numbers from caecum to rectum. Paneth cells were not seen in the distal colon in the control group, but they were present there in 11 of 13 patients with ulcerative colitis and 14 of 15 with Crohn’s disease. Only patients with IBD showed Paneth cell hyperplasia, assessed as more than 10 Paneth cells per 10 well-oriented crypts at any site. There was a statistically significant increase in Paneth cells in the caecum, ascending, transverse and descending colon in UC and in the ascending, transverse, descending and sigmoid colon in CD compared with controls. There was no significant difference between UC and CD. There was no correlation between the site of PCM and acute or chronic inflammation, crypt distortion or eosinophilia.ConclusionPaneth cells are found in the proximal but not the distal colon in otherwise normal paediatric colonic series. A high proportion of UC and CD patients show PCM in the distal colon. This is present early in the disease and does not correlate with histological features of chronicity.

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Intestinal alpha-defensin expression in pediatric inflammatory bowel disease1

Cited by 27 publications

References 29 publications

The role of innate immune-stimulated epithelial apoptosis during gastrointestinal inflammatory diseases

The role of innate immune-stimulated epithelial apoptosis during gastrointestinal inflammatory diseases

Terminal Restriction Fragment Length Polymorphism Analysis of the Gut Microbiota Profiles of Pediatric Patients with Inflammatory Bowel Disease

Paneth cell metaplasia in newly diagnosed inflammatory bowel disease in children

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