{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["10"],"submitter":["Lindemann A"],"pubmed_abstract":["<h4>Background and aims</h4>Acute severe steroid-refractory ulcerative colitis remains a medically challenging condition with frequent need of surgery. It can be treated with the calcineurin inhibitor cyclosporine A with the need for therapeutic drug monitoring and significant toxicity. Recently, a novel calcineurin inhibitor, voclosporin, has been approved for the treatment of lupus nephritis with no need for therapeutic drug monitoring and an improved long-term safety profile. However, the therapeutic effect of voclosporin in acute severe steroid-refractory ulcerative colitis is still uncertain. We aimed to assess the therapeutic potential of voclosporin to ameliorate inflammation in an experimental model of colitis.<h4>Methods</h4>We used the dextran sodium sulfate-induced model of colitis in C57BL/6 J wildtype mice treated with either cyclosporine A, voclosporin or solvent control. We employed endoscopy, histochemistry, immunofluorescence, bead-based multiplex immunoassays and flow cytometry to study the therapeutic effect of calcineurin inhibitors in a preventive setting.<h4>Results</h4>Acute colitis was induced by dextran sodium sulfate characterized by weight loss, diarrhea, mucosal erosions and rectal bleeding. Both cyclosporine A and voclosporin strongly ameliorated the course of disease and reduced colitis severity in a similar manner.<h4>Conclusion</h4>Voclosporin was identified as biologically effective in a preclinical model of colitis and may be a potential therapeutic option in treating acute severe steroid-refractory ulcerative colitis."],"journal":["Frontiers in medicine"],"pagination":["1177450"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10289195"],"repository":["biostudies-literature"],"pubmed_title":["Protective effect of the novel calcineurin inhibitor voclosporin in experimental colitis."],"pmcid":["PMC10289195"],"pubmed_authors":["Neurath MF","Lindemann A","Zundler S","Roth D","Koop K","Neufert C","Leppkes M","Atreya R"],"additional_accession":[]},"is_claimable":false,"name":"Protective effect of the novel calcineurin inhibitor voclosporin in experimental colitis.","description":"<h4>Background and aims</h4>Acute severe steroid-refractory ulcerative colitis remains a medically challenging condition with frequent need of surgery. It can be treated with the calcineurin inhibitor cyclosporine A with the need for therapeutic drug monitoring and significant toxicity. Recently, a novel calcineurin inhibitor, voclosporin, has been approved for the treatment of lupus nephritis with no need for therapeutic drug monitoring and an improved long-term safety profile. However, the therapeutic effect of voclosporin in acute severe steroid-refractory ulcerative colitis is still uncertain. We aimed to assess the therapeutic potential of voclosporin to ameliorate inflammation in an experimental model of colitis.<h4>Methods</h4>We used the dextran sodium sulfate-induced model of colitis in C57BL/6 J wildtype mice treated with either cyclosporine A, voclosporin or solvent control. We employed endoscopy, histochemistry, immunofluorescence, bead-based multiplex immunoassays and flow cytometry to study the therapeutic effect of calcineurin inhibitors in a preventive setting.<h4>Results</h4>Acute colitis was induced by dextran sodium sulfate characterized by weight loss, diarrhea, mucosal erosions and rectal bleeding. Both cyclosporine A and voclosporin strongly ameliorated the course of disease and reduced colitis severity in a similar manner.<h4>Conclusion</h4>Voclosporin was identified as biologically effective in a preclinical model of colitis and may be a potential therapeutic option in treating acute severe steroid-refractory ulcerative colitis.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023","modification":"2024-11-13T10:27:29.474Z","creation":"2024-11-13T10:27:29.474Z"},"accession":"S-EPMC10289195","cross_references":{"pubmed":["37358998"],"doi":["10.3389/fmed.2023.1177450"]}}