Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a lipidomic study

Abstract Background Mechanisms causing non-response to biological agents in IBD remain to be fully understood. Thus, we aimed to characterize the lipid profile in treatment refractory non-immunogenic patients with adequate trough-levels. Methods Patients with IBD refractory to treatment with anti-tu...

Full description

Saved in:
Bibliographic Details
Main Authors: Øystein K. Moe, Qian Gao, Dawei Geng, Einar Jensen, Rasmus Goll, Oddmund Nestegard, Mona D. Gundersen, Jon R. Florholmen, T. Moritz
Format: Article
Language:English
Published: BMC 2025-05-01
Series:BMC Gastroenterology
Subjects:
Online Access:https://doi.org/10.1186/s12876-025-03944-6
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849731819406098432
author Øystein K. Moe
Qian Gao
Dawei Geng
Einar Jensen
Rasmus Goll
Oddmund Nestegard
Mona D. Gundersen
Jon R. Florholmen
T. Moritz
author_facet Øystein K. Moe
Qian Gao
Dawei Geng
Einar Jensen
Rasmus Goll
Oddmund Nestegard
Mona D. Gundersen
Jon R. Florholmen
T. Moritz
author_sort Øystein K. Moe
collection DOAJ
description Abstract Background Mechanisms causing non-response to biological agents in IBD remain to be fully understood. Thus, we aimed to characterize the lipid profile in treatment refractory non-immunogenic patients with adequate trough-levels. Methods Patients with IBD refractory to treatment with anti-tumour necrosis factor or vedolizumab were included from a Norwegian translation study. Mucosal lipid profiles were compared to reference groups. The reference groups included treatment naïve IBD patients with moderate to severe disease at debut who later achieved remission or response on antiTNFs, IBD patients treated to remission with biological agents, and healthy normal controls. Lipidomics analyses were performed on mucosal biopsies. Statistical analyses of lipid levels were carried out using generalized least squares. Lipidomics data were log2-transformed and auto-scaled before analysis. P-values were adjusted using Benjamini- Hochberg procedure to control the false discovery rate (FDR). Results Proinflammatory lipids including ceramides and sphingomyelins and protective lipids like glycerophosphocholines and glycerophosphoethanolamines were significantly decreased in treatment refractory UC patients compared to treatment naïve UC patients with moderate to severe disease. Compared to controls, major changes in ceramides (Cer), hexosyl ceramides (HexCer), sphingomyelins (SM), glycerophosphocholines (PC), glycerophosphoethanolamines (PE) and glycerophosphoserines (PS) were observed in treatment refractory UC patients. Refractory CD patients showed minor changes compared to the other CD-groups. There were no significant differences in the mucosal lipid levels of IBD patients in remission compared to normal controls. Conclusions The mucosal lipid profile of treatment refractory UC shows marked shifts compared to treatment naïve UC at debut with moderate to severe inflammation. These are novel findings which possibly indicate dynamic processes of long-standing mucosal inflammation. The mucosal lipid profile of IBD patients in remission seems to be similar to the normal state.
format Article
id doaj-art-be8c3b916f7945a58f050ea109da3cc5
institution DOAJ
issn 1471-230X
language English
publishDate 2025-05-01
publisher BMC
record_format Article
series BMC Gastroenterology
spelling doaj-art-be8c3b916f7945a58f050ea109da3cc52025-08-20T03:08:25ZengBMCBMC Gastroenterology1471-230X2025-05-0125111110.1186/s12876-025-03944-6Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a lipidomic studyØystein K. Moe0Qian Gao1Dawei Geng2Einar Jensen3Rasmus Goll4Oddmund Nestegard5Mona D. Gundersen6Jon R. Florholmen7T. Moritz8Research Group of Gastroenterology and Nutrition, Department of Clinical Medicine, UiT The Arctic University of NorwayNovo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of CopenhagenNovo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of CopenhagenNatural Products and Medicinal Chemistry Research Group, Department of Pharmacy Faculty of Health Sciences, UiT The Arctic University of NorwayResearch Group of Gastroenterology and Nutrition, Department of Clinical Medicine, UiT The Arctic University of NorwayResearch Group of Gastroenterology and Nutrition, Department of Clinical Medicine, UiT The Arctic University of NorwayResearch Group of Gastroenterology and Nutrition, Department of Clinical Medicine, UiT The Arctic University of NorwayResearch Group of Gastroenterology and Nutrition, Department of Clinical Medicine, UiT The Arctic University of NorwayNovo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of CopenhagenAbstract Background Mechanisms causing non-response to biological agents in IBD remain to be fully understood. Thus, we aimed to characterize the lipid profile in treatment refractory non-immunogenic patients with adequate trough-levels. Methods Patients with IBD refractory to treatment with anti-tumour necrosis factor or vedolizumab were included from a Norwegian translation study. Mucosal lipid profiles were compared to reference groups. The reference groups included treatment naïve IBD patients with moderate to severe disease at debut who later achieved remission or response on antiTNFs, IBD patients treated to remission with biological agents, and healthy normal controls. Lipidomics analyses were performed on mucosal biopsies. Statistical analyses of lipid levels were carried out using generalized least squares. Lipidomics data were log2-transformed and auto-scaled before analysis. P-values were adjusted using Benjamini- Hochberg procedure to control the false discovery rate (FDR). Results Proinflammatory lipids including ceramides and sphingomyelins and protective lipids like glycerophosphocholines and glycerophosphoethanolamines were significantly decreased in treatment refractory UC patients compared to treatment naïve UC patients with moderate to severe disease. Compared to controls, major changes in ceramides (Cer), hexosyl ceramides (HexCer), sphingomyelins (SM), glycerophosphocholines (PC), glycerophosphoethanolamines (PE) and glycerophosphoserines (PS) were observed in treatment refractory UC patients. Refractory CD patients showed minor changes compared to the other CD-groups. There were no significant differences in the mucosal lipid levels of IBD patients in remission compared to normal controls. Conclusions The mucosal lipid profile of treatment refractory UC shows marked shifts compared to treatment naïve UC at debut with moderate to severe inflammation. These are novel findings which possibly indicate dynamic processes of long-standing mucosal inflammation. The mucosal lipid profile of IBD patients in remission seems to be similar to the normal state.https://doi.org/10.1186/s12876-025-03944-6Biological therapyInflammatory bowel diseaseNon-responseLipids
spellingShingle Øystein K. Moe
Qian Gao
Dawei Geng
Einar Jensen
Rasmus Goll
Oddmund Nestegard
Mona D. Gundersen
Jon R. Florholmen
T. Moritz
Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a lipidomic study
BMC Gastroenterology
Biological therapy
Inflammatory bowel disease
Non-response
Lipids
title Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a lipidomic study
title_full Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a lipidomic study
title_fullStr Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a lipidomic study
title_full_unstemmed Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a lipidomic study
title_short Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a lipidomic study
title_sort marked mucosal lipid shifts in treatment refractory inflammatory bowel disease a lipidomic study
topic Biological therapy
Inflammatory bowel disease
Non-response
Lipids
url https://doi.org/10.1186/s12876-025-03944-6
work_keys_str_mv AT øysteinkmoe markedmucosallipidshiftsintreatmentrefractoryinflammatoryboweldiseasealipidomicstudy
AT qiangao markedmucosallipidshiftsintreatmentrefractoryinflammatoryboweldiseasealipidomicstudy
AT daweigeng markedmucosallipidshiftsintreatmentrefractoryinflammatoryboweldiseasealipidomicstudy
AT einarjensen markedmucosallipidshiftsintreatmentrefractoryinflammatoryboweldiseasealipidomicstudy
AT rasmusgoll markedmucosallipidshiftsintreatmentrefractoryinflammatoryboweldiseasealipidomicstudy
AT oddmundnestegard markedmucosallipidshiftsintreatmentrefractoryinflammatoryboweldiseasealipidomicstudy
AT monadgundersen markedmucosallipidshiftsintreatmentrefractoryinflammatoryboweldiseasealipidomicstudy
AT jonrflorholmen markedmucosallipidshiftsintreatmentrefractoryinflammatoryboweldiseasealipidomicstudy
AT tmoritz markedmucosallipidshiftsintreatmentrefractoryinflammatoryboweldiseasealipidomicstudy