Expression of zebrafish cxcl8 (interleukin-8) and its receptors during development and in response to immune stimulation

Oehlers, Stefan H.; Flores, Maria Vega; Hall, Cathy W.; O’Toole, Ronan; Swift, Simon; Crosier, Kathryn E.; Crosier, Philip S.

doi:10.1016/j.dci.2009.11.007

Cited by 124 publications

(92 citation statements)

References 44 publications

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“…Considering the multifaceted and central role of IL-6 in a number of inflammatory conditions, including IBD [39], the results are not readily explained, but knowledge of IL-6 function and signaling is considered to be inadequate in fish at present [40]. Confirming earlier zebrafish-inflammatory studies [8] [9] [10] [41], the neutrophil-activating chemokineCxCL8 (IL-8) was significantly up-regulated in the TNBS groups after 72 hpi. In the oxazolone-exposed group, CxCL8 transcript levels were also elevated after 72 hpi, albeit at noticeably higher level than in the TNBS group.…”

Section: Discussionsupporting

confidence: 66%

“…In the oxazolone-exposed group, CxCL8 transcript levels were also elevated after 72 hpi, albeit at noticeably higher level than in the TNBS group. Cxcl8 is pivotal in orchestrating neutrophil influx to the site of inflammation, and gene trancripts have been detected from intestinal cells in larval zebrafish in a TNBS-model [8]. As noted by Brugman [22], mice do not possess a Cxcl8 gene that is homologous to its human counterpart CXCL8, in contrast to zebrafish.…”

Section: Discussionmentioning

confidence: 97%

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Comparison of Two Chemically-Induced Colitis-Models in Adult Zebrafish, Using Optical Projection Tomography and Novel Transcriptional Markers

Haarder¹,

Kania²,

Holm³

et al. 2016

OJI

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Crohn's disease and ulcerative colitis-inflammatory bowel diseases (IBD)-are chronic conditions with an inadequately understood pathogenesis. Employing a set of novel molecular markers in a gene expression assay (qPCR), we have used adult zebrafish to investigate two acute inflammatory models, induced by the haptenizing agents oxazolone and TNBS. In addition, goblet cell dynamics in the scales and intestine and 5-HT (serotonin) in intestinal tissues were investigated through optical projection tomography. Gene expression studies revealed a distinct and significant upregulation of proinflammatory cytokines, acute-phase reactants and metalloprotease 9 in both chemical models, primarily after 72 hours. In comparison, transcription factors and cytokines associated with Th1 and Th17 (Crohn's) and Th2 (ulcerative colitis) were mainly not affected in this acute setting. However, elevated transcript levels were detected in Foxp3, IL-10 and T-bet, which are linked with tolerance and Tregs in mammals. Goblet cells in scales were depleted in both chemical models and in the intestine of oxazolone-treated fish. A marked 5-HT signal was noted in intestinal tissue of some chemically treated zebrafish. In conclusion, a distinct acute inflammatory reaction was induced in both chemical models. Further, oxazolone and TNBS did not result in clear-cut Th2 and Th1/Th17 pathway signaling at this early timepoint, but the applied molecular tools may provide further insight to the IBD pathogenesis and translational value of the IBD zebrafish model. How to cite this paper:

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 97%

Comparison of Two Chemically-Induced Colitis-Models in Adult Zebrafish, Using Optical Projection Tomography and Novel Transcriptional Markers

Haarder¹,

Kania²,

Holm³

et al. 2016

OJI

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“…Because of the substantial difference in the biological role of TNF-a in mammals and zebrafish, we examined the transcription of a panel of pro-inflammatory cytokines as a more accurate measure of inflammation (Roca et al, 2008). Consistent with previous studies of zebrafish larval intestinal infection, an early induction of pro-inflammatory cytokine transcription has been observed in this model (Oehlers et al, 2010). Because Fig.…”

Section: Microbiota Is Necessary For the Induction Of Inflammation Bysupporting

confidence: 50%

“…A range of TNBS doses were investigated with the aim of establishing a dose that would not cause overt morphological changes to larvae while reproducibly inducing inflammation (Fleming et al, 2010;Oehlers et al, 2010). Initial titration studies showed a dose of up to 50 mg/ml TNBS could be tolerated for three continuous days with greater than 90% cohort survival while doses of 75 mg/ml or greater resulted in less than 50% survival by three post-exposure (data not shown).…”

Section: Histological Analysis Of Tnbs-induced Enterocolitismentioning

confidence: 99%

“…Previous study of the TNBS-exposure model had revealed an up-regulation of pro-inflammatory cytokine genes at the whole organism level (Oehlers et al, 2010), we carried out dissections to resolve the relative responsiveness of the body and gut to TNBS exposure. We found both compartments significantly up-regulated transcription of il-1b (Fig.…”

Section: Tnbs Exposure Primarily Evokes An Inflammatory Response Withmentioning

confidence: 99%

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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

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164

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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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Zebrafish heat shock protein a4 genes in the intestinal epithelium are up‐regulated during inflammation

Crawford

Flores

Oehlers

et al. 2011

Genesis

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A number of heat shock proteins (HSPs), including Hsp70 and Hsp110, function as molecular chaperones within intestinal epithelial cells that line the mammalian digestive system. HSPs confer cellular protection against environmental stress induced by chemical toxins or pathogens. There is interest in how members of this protein family might influence the progression of inflammatory bowel disease. Using the zebrafish model system, we report the expression of the duplicated hspa4 genes within the intestinal epithelium. The hspa4 genes belong to the Hsp110 family. We show that under inflammatory stress conditions within the gut, expression of these genes is up-regulated in a similar manner to that previously observed for mammalian Hsp70. Because of the amenability of the zebrafish to whole-animal screening protocols, the hspa4 genes could be used as effective read-outs for genetic, chemical and environmental factors that might influence intestinal inflammation.

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Expression of zebrafish cxcl8 (interleukin-8) and its receptors during development and in response to immune stimulation

Cited by 124 publications

References 44 publications

Comparison of Two Chemically-Induced Colitis-Models in Adult Zebrafish, Using Optical Projection Tomography and Novel Transcriptional Markers

Comparison of Two Chemically-Induced Colitis-Models in Adult Zebrafish, Using Optical Projection Tomography and Novel Transcriptional Markers

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

Zebrafish heat shock protein a4 genes in the intestinal epithelium are up‐regulated during inflammation

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