Increased Expression of CCL20 in Human Inflammatory Bowel Disease

Kaser, Arthur; Ludwiczek, Othmar; Holzmann, Sandra; Moschen, Alexander R.; Weiss, Günter; Enrich, Barbara; Graziadei, Ivo; Dunzendorfer, Stefan; Wiedermann, Christian J.; Mürzl, Elisabeth; Grasl, Eveline; Jasarevic, Zerina; Romani, Nikolaus; Offner, Felix; Tilg, Herbert

doi:10.1023/b:joci.0000018066.46279.6b

Cited by 181 publications

(144 citation statements)

References 59 publications

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“…2E). We did not observe an induction of ccl20 transcription in the gut of zebrafish larvae exposed to TNBS, in contrast with that reported from studies with IBD patients (Kwon et al, 2002;Kaser et al, 2004). Transcription of the chemotactic cytokine il-8, known to be upregulated in IBD (Daig et al, 1996), was significantly increased in the intestine but not the body of larval zebrafish exposed to TNBS.…”

Section: Tnbs Exposure Primarily Evokes An Inflammatory Response Withcontrasting

confidence: 99%

A chemical enterocolitis model in zebrafish larvae that is dependent on microbiota and responsive to pharmacological agents

Oehlers

Flores

Okuda

et al. 2010

Developmental Dynamics

120

168

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Inflammatory bowel disease (IBD) results from dysfunctional interactions between the intestinal immune system and microbiota, influenced by host genetic susceptibility. Because a key feature of the pathology is intestinal epithelial damage, potential disease factors have been traditionally analyzed within the background of chemical colitis models in mice. The zebrafish has greatly complemented the mouse for modeling aspects of disease processes, with an advantage for high content drug screens. Larval zebrafish exposed to the haptenizing agent trinitrobenzene sulfonic acid (TNBS) displayed impaired intestinal homeostasis and inflammation reminiscent of human IBD. There was a marked induction of pro-inflammatory cytokines, the degradative enzyme mmp9 and leukocytosis. Enterocolitis was dependent on microbiota and Toll-like receptor signaling, that can be ameliorated by antibiotic and anti-inflammatory drug treatments. This system will be useful to rapidly interrogate in vivo the biological significance of the IBD candidate genes so far identified and to carry out pharmacological modifier screens. Developmental Dynamics 240:288-298,

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Section: Tnbs Exposure Primarily Evokes An Inflammatory Response Withcontrasting

confidence: 99%

A chemical enterocolitis model in zebrafish larvae that is dependent on microbiota and responsive to pharmacological agents

Oehlers

Flores

Okuda

et al. 2010

Developmental Dynamics

120

168

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“…CCL20 shows no effect on peritoneal macrophages and CLP-induced mortality CCL20, the only chemokine ligand for CCR6, is upregulated during inflammation [30,31] and by specific proinflammatory cytokines [32]. An increase in CCL20 level in the peritoneal cavity was observed in WT mice with CLP-induced peritonitis with a peak at 24 h (Fig.…”

Section: Leukocyte Recruitment Into the Peritoneal Cavity Post Clp-inmentioning

confidence: 90%

The chemokine receptor CCR6 is an important component of the innate immune response

et al. 2007

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In our initial studies we found that naïve CCR6‐deficient (CCR6–/–) C57BL/6 mice possessed significantly lower number of both F4/80+ macrophages and dendritic cells (DC), but higher number of B cells in the peritoneal cavity, as compared to naïve wild type (WT) controls. Furthermore, peritoneal macrophages isolated from CCR6–/– mice expressed significantly lower levels of inflammatory cytokines and nitric oxide following lipopolysaccharide (LPS)stimulation, as compared to WT macrophages. In a severe experimental peritonitis model induced by cecal ligation and puncture (CLP), CCR6–/– mice were protected when compared with WT controls. At 24 h following the induction of peritonitis, CCR6–/– mice exhibited significantly lower levels of inflammatory cytokines/chemokines in both the peritoneal cavity and blood. Interestingly, DC recruitment into the peritoneal cavity was impaired in CCR6–/– mice during the evolution of CLP‐induced peritonitis. Peritoneal macrophages isolated from surviving CCR6–/– mice 3 days after CLP‐induced peritonitis exhibited an enhanced LPS response compared with similarly treated WT peritoneal macrophages. These data illustrate that CCR6 deficiency alters the innate response via attenuating the hyperactive local and systemic inflammatory response during CLP‐induced peritonitis.

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“…Another fact identified by them was that TNF-α had served to increase CCL20 secretion in the healthy controls whilst anti-TNF -α acted to decrease it. This study had illustrated the contribution of CCL20 in regulating the mobilization of T lymphocytes and antigen sampling cell populations into the gut mucosa during IBD [72].…”

Section: The Effect Of Dendritic Cells (Dc)mentioning

confidence: 87%

CCR6-CCL20 Axis in IBD: What have we learnt in the past 20 years?

Ranasinghe¹,

Eri²

2018

Preprint

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Inflammatory bowel disease (IBD) is a CC chemokine receptor 6 (CCR6) -associated immune mediated disorder which has attracted an extensive superfluity of experimental analyses. IBD has come to the fore of varied scrutinizing owing to its complexity by nature for comprising of two synergistic sub phenotypes; Crohn's disease (CD) and Ulcerative colitis (UC). Both these disease entities cause potent immune dysregulation followed by intense tissue damage within the gut mucosal system, initiating symptoms which are severely debilitating. Multiple causative factors are said to be responsible for IBD but direct immune dysfunction is kindled by overplay of innate and adaptive immune responses produced against a pathogenic microbial attack through the weakened or leaky gut epithelial barrier. Once immune homeostasis is not achieved by tolerating agents, the self-assertive adaptive immunity mobilize its various T and B cell cohorts initializing their allied immune mechanisms by vigorously deploying them towards the site of infection. CCR6 and its unique solitary ligand CC-chemokine ligand 20 (CCL20) are small protein molecules which are abundantly expressed by T and B lymphocytes and act as chemotactic immune-modulatory envoys that help in the deployment of the effector lymphocyte arm of the immune system, producing two directly opposing outcomes in IBD. This dichotomous immunity consists of either immune tolerance or inflammation which then develops into a chronic state, remaining catatonic to inherent immunity or targeted clinical therapy. In this review, we have chronologically identified a plethora of experimental studies radiating into 14 different compartments highlighted in the visual depiction which have employed both mouse models and clinical subjects spanning a period of nearly two decades. In doing so, we expect the research community would further benefit by tracing through the history, thereby understanding the CCR6 -CCL20 axis in IBD and identifying the gaps in literature which can be fortuitously filled in the future.Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted:

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Increased Expression of CCL20 in Human Inflammatory Bowel Disease

Cited by 181 publications

References 59 publications

A chemical enterocolitis model in zebrafish larvae that is dependent on microbiota and responsive to pharmacological agents

A chemical enterocolitis model in zebrafish larvae that is dependent on microbiota and responsive to pharmacological agents

The chemokine receptor CCR6 is an important component of the innate immune response

CCR6-CCL20 Axis in IBD: What have we learnt in the past 20 years?

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