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Article ; Online: TNFα-Antagonist Use and Mucosal Inflammation Are Associated with Increased Intestinal Expression of SARS-CoV-2 Host Protease TMPRSS2 in Patients with Inflammatory Bowel Disease.

Bangma, Amber / Voskuil, Michiel D / Weersma, Rinse K

2020 Volume 160, Issue 7, Page(s) 2621–2622

MeSH term(s)	COVID-19 ; Humans ; Inflammation ; Inflammatory Bowel Diseases ; Peptide Hydrolases ; Peptidyl-Dipeptidase A ; SARS-CoV-2 ; Serine Endopeptidases ; Tumor Necrosis Factor-alpha
Chemical Substances	Tumor Necrosis Factor-alpha ; Peptide Hydrolases (EC 3.4.-) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; Serine Endopeptidases (EC 3.4.21.-) ; TMPRSS2 protein, human (EC 3.4.21.-)
Keywords	covid19
Language	English
Publishing date	2020-06-15
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2020.05.091
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Zs.MO 572: Show issues

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Article ; Online: Reply.

Uniken Venema, Werna T / Voskuil, Michiel D / Festen, Eleonora A

Gastroenterology

2019 Volume 157, Issue 1, Page(s) 266–267

Language	English
Publishing date	2019-05-28
Publishing country	United States
Document type	Letter
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2019.05.045
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Article ; Online: Polygenetic risk scores do not add predictive power to clinical models for response to anti-TNFα therapy in inflammatory bowel disease.

Karmi, Naomi / Bangma, Amber / Spekhorst, Lieke M / van Dullemen, Hendrik M / Visschedijk, Marijn C / Dijkstra, Gerard / Weersma, Rinse K / Voskuil, Michiel D / Festen, Eleonora A M

PloS one

2021 Volume 16, Issue 9, Page(s) e0256860

Abstract: Background: Anti-tumour necrosis factor alpha (TNFα) therapy is widely used in the management of Crohn's disease (CD) and ulcerative colitis (UC). However, up to a third of patients do not respond to induction therapy and another third of patients lose ... ...

Abstract	Background: Anti-tumour necrosis factor alpha (TNFα) therapy is widely used in the management of Crohn's disease (CD) and ulcerative colitis (UC). However, up to a third of patients do not respond to induction therapy and another third of patients lose response over time. To aid patient stratification, polygenetic risk scores have been identified as predictors of response to anti-TNFα therapy. We aimed to replicate the association between polygenetic risk scores and response to anti-TNFα therapy in an independent cohort of patients, to establish its clinical validity. Materials and methods: Primary non-response, primary response, durable response and loss of response to anti-TNFα therapy was retrospectively assessed for each patient using stringent definitions. Genome wide genotyping was performed and previously described polygenetic risk scores for primary non-response and durable response were calculated. We compared polygenetic risk scores between patients with primary response and primary non-response, and between patients with durable response and loss of response, using separate analyses for CD and UC. Results: Out of 334 patients with CD, 15 (4%) patients met criteria for primary non-response, 221 (66%) for primary response, 115 (34%) for durable response and 35 (10%) for loss of response. Out of 112 patients with UC, 12 (11%) met criteria for primary non-response, 68 (61%) for primary response, 19 (17%) for durable response and 20 (18%) for loss of response. No significant differences in polygenetic risk scores were found between primary non-responders and primary responders, and between durable responders and loss of responders. Conclusions: We could not replicate the previously reported association between polygenetic risk scores and response to anti-TNFα therapy in an independent cohort of patients with CD or UC. Currently, there is insufficient evidence to use polygenetic risk scores to predict response to anti-TNFα therapy in patients with IBD.
MeSH term(s)	Adalimumab/therapeutic use ; Adult ; Colitis, Ulcerative/drug therapy ; Colitis, Ulcerative/genetics ; Colitis, Ulcerative/immunology ; Colitis, Ulcerative/pathology ; Crohn Disease/drug therapy ; Crohn Disease/genetics ; Crohn Disease/immunology ; Crohn Disease/pathology ; Female ; Gastrointestinal Agents/therapeutic use ; Gene Expression ; Humans ; Immunologic Factors/therapeutic use ; Immunotherapy/methods ; Infliximab/therapeutic use ; Male ; Middle Aged ; Multifactorial Inheritance ; Remission Induction ; Retrospective Studies ; Treatment Outcome ; Tumor Necrosis Factor-alpha/antagonists & inhibitors ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Gastrointestinal Agents ; Immunologic Factors ; Tumor Necrosis Factor-alpha ; Infliximab (B72HH48FLU) ; Adalimumab (FYS6T7F842)
Language	English
Publishing date	2021-09-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0256860
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Article ; Online: The Composition and Metabolic Potential of the Human Small Intestinal Microbiota Within the Context of Inflammatory Bowel Disease.

Ruigrok, Renate A A A / Collij, Valerie / Sureda, Paula / Klaassen, Marjolein A Y / Bolte, Laura A / Jansen, Bernadien H / Voskuil, Michiel D / Fu, Jingyuan / Wijmenga, Cisca / Zhernakova, Alexandra / Weersma, Rinse K / Vich Vila, Arnau

Journal of Crohn's & colitis

2021 Volume 15, Issue 8, Page(s) 1326–1338

Abstract: Background and aims: The human gastrointestinal tract harbours distinct microbial communities essential for health. Little is known about small intestinal communities, despite the small intestine playing a fundamental role in nutrient absorption and ... ...

Abstract	Background and aims: The human gastrointestinal tract harbours distinct microbial communities essential for health. Little is known about small intestinal communities, despite the small intestine playing a fundamental role in nutrient absorption and host-microbe immune homeostasis. We aimed to explore the small intestine microbial composition and metabolic potential, in the context of inflammatory bowel disease [IBD]. Methods: Metagenomes derived from faecal samples and extensive phenotypes were collected from 57 individuals with an ileostomy or ileoanal pouch, and compared with 1178 general population and 478 IBD faecal metagenomes. Microbiome features were identified using MetaPhAn2 and HUMAnN2, and association analyses were performed using multivariate linear regression. Results: Small intestinal samples had a significantly lower bacterial diversity, compared with the general population and, to a lesser extent, IBD samples. Comparing bacterial composition, small intestinal samples clustered furthest from general population samples and closest to IBD samples with intestinal resections. Veillonella atypica, Streptococcus salivarius, and Actinomyces graevenitzii were among the species significantly enriched in the small intestine. Predicted metabolic pathways in the small intestine are predominantly involved in simple carbohydrate and energy metabolism, but also suggest a higher pro-inflammatory potential. Conclusions: We described the bacterial composition and metabolic potential of the small intestinal microbiota. The colonic microbiome of IBD patients, particularly with intestinal resections, showed resemblance to that of the small intestine. Moreover, several features characterising the small intestinal microbiome have been previously associated with IBD. These results highlight the importance of studying the small intestinal microbiota to gain new insight into disease pathogenesis.
MeSH term(s)	Cohort Studies ; Feces/microbiology ; Female ; Gastrointestinal Microbiome ; Humans ; Inflammatory Bowel Diseases ; Intestine, Small/microbiology ; Male ; Middle Aged
Language	English
Publishing date	2021-01-29
Publishing country	England
Document type	Comparative Study ; Journal Article
ZDB-ID	2390120-2
ISSN	1876-4479 ; 1873-9946
ISSN (online)	1876-4479
ISSN	1873-9946
DOI	10.1093/ecco-jcc/jjab020
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Article ; Online: The genetic background of inflammatory bowel disease: from correlation to causality.

Uniken Venema, Werna Tc / Voskuil, Michiel D / Dijkstra, Gerard / Weersma, Rinse K / Festen, Eleonora Am

The Journal of pathology

2017 Volume 241, Issue 2, Page(s) 146–158

Abstract: Recent studies have greatly improved our insight into the genetic background of inflammatory bowel disease (IBD). New high-throughput technologies and large-scale international collaborations have contributed to the identification of 200 independent ... ...

Abstract	Recent studies have greatly improved our insight into the genetic background of inflammatory bowel disease (IBD). New high-throughput technologies and large-scale international collaborations have contributed to the identification of 200 independent genetic risk loci for IBD. However, in most of these loci, it is unclear which gene conveys the risk for IBD. More importantly, it is unclear which variant within or near the gene is causal to the disease. Using targeted GWAS, imputation, resequencing of risk loci, and in silico fine-mapping of densely typed loci, several causal variants have been identified in IBD risk genes, and various pathological pathways have been uncovered. Current research in the field of IBD focuses on the effect of these causal variants on gene expression and protein function. However, more elements than only the genome must be taken into account to disentangle the multifactorial pathology of IBD. The genetic risk loci identified to date only explain a small part of genetic variance in disease risk. Currently, large multi-omics studies are incorporating factors ranging from the gut microbiome to the environment. In this review, we present the progress that has been made in IBD genetic research and stress the importance of studying causality to increase our understanding of the pathogenesis of IBD. We highlight important causal genetic variants in the candidate genes NOD2, ATG16L1, IRGM, IL23R, CARD9, RNF186, and PRDM1. We describe their downstream effects on protein function and their direct effects on the gut immune system. Furthermore, we discuss the future role of genetics in unravelling disease mechanisms in IBD. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
MeSH term(s)	Animals ; Crohn Disease/genetics ; Genetic Background ; Genetic Predisposition to Disease ; Genetic Variation/genetics ; Genome-Wide Association Study/methods ; Humans ; Inflammatory Bowel Diseases/genetics
Language	English
Publishing date	2017-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	3119-7
ISSN	1096-9896 ; 0022-3417
ISSN (online)	1096-9896
ISSN	0022-3417
DOI	10.1002/path.4817
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Article ; Online: Environmental factors associated with biological use and surgery in inflammatory bowel disease.

van der Sloot, Kimberley W J / Geertsema, Paul / Rijkmans, Hanneke C / Voskuil, Michiel D / van Dullemen, Hendrik M / Visschedijk, Marijn C / Festen, Eleonora A M / Weersma, Rinse K / Alizadeh, Behrooz Z / Dijkstra, Gerard

Journal of gastroenterology and hepatology

2020 Volume 36, Issue 4, Page(s) 1022–1034

Abstract: Background and aim: While major efforts were made studying the complex etiology of inflammatory bowel disease (IBD) including environmental factors, less is known about underlying causes leading to the heterogeneous and highly variable course of disease. ...

Abstract	Background and aim: While major efforts were made studying the complex etiology of inflammatory bowel disease (IBD) including environmental factors, less is known about underlying causes leading to the heterogeneous and highly variable course of disease. As cigarette smoking cessation is the best-known environmental factor with beneficial effect in Crohn's disease (CD), more exposome factors are likely involved. Further insights into the role of the exposome in heterogeneity of disease might not only further knowledge of underlying pathways, but also allow for better risk stratification. Methods: Seven hundred twenty-eight IBD patients completed the validated Groningen IBD Environmental Questionnaire, collecting exposome data for 93 exposome factors. Associations with disease course, that is, for need for surgery or biological therapy, were evaluated using univariate and multivariate-adjusted logistic regression modeling. Results: No significant associations were seen after Bonferroni correction. However, 11 novel exposome factors were identified with P < 0.05. Two factors were associated with course of CD and ulcerative colitis (UC): beer (CD OR0.3/UC OR0.3) and cannabis (0.5/2.2). While in CD, carpet flooring (0.5) was associated with biological use, and four factors were associated with surgery: working shifts (1.8), appendectomy (2.4), frequent tooth brushing (2.8), and large household size (0.1). For UC, migrants more often required biologicals (10.2). Childhood underweight (3.4), amphetamine use (6.2), and cocaine use (4.8) were associated with surgery. Five factors were replicated. Conclusions: We identified 16 environmental factors nominally associated with biological use and surgery in established IBD. These new insights form an important stepping stone to guide research on biological pathways involved, risk stratification, tailor-made interventions, and preventive strategies in IBD.
MeSH term(s)	Adult ; Appendectomy ; Beer/adverse effects ; Biological Factors/therapeutic use ; Cannabis/adverse effects ; Cigarette Smoking/adverse effects ; Colitis, Ulcerative/drug therapy ; Colitis, Ulcerative/etiology ; Colitis, Ulcerative/prevention & control ; Colitis, Ulcerative/surgery ; Crohn Disease/drug therapy ; Crohn Disease/etiology ; Crohn Disease/prevention & control ; Crohn Disease/surgery ; Exposome ; Female ; Floors and Floorcoverings ; Humans ; Male ; Middle Aged ; Risk ; Shift Work Schedule/adverse effects ; Smoking Cessation ; Surveys and Questionnaires ; Toothbrushing
Chemical Substances	Biological Factors
Language	English
Publishing date	2020-09-23
Publishing country	Australia
Document type	Journal Article
ZDB-ID	632882-9
ISSN	1440-1746 ; 0815-9319
ISSN (online)	1440-1746
ISSN	0815-9319
DOI	10.1111/jgh.15223
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Zs.A 2180: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Latent cytomegalovirus infection does not influence long-term disease outcomes in inflammatory bowel disease, but is associated with later onset of disease.

van der Sloot, Kimberley W J / Voskuil, Michiel D / Visschedijk, Marijn C / Festen, Eleonora A M / van Dullemen, Hendrik M / Weersma, Rinse K / Alizadeh, Behrooz Z / van Leer-Buter, Coretta / Dijkstra, Gerard

Scandinavian journal of gastroenterology

2020 Volume 55, Issue 8, Page(s) 891–896

Abstract: Objectives: Cytomegalovirus (CMV) infection is common in the general population. CMV infection negatively affects disease course in transplant recipients and HIV patients. Whereas primary CMV infections may occur sporadically in seronegative patients, ... ...

Abstract	Objectives: Cytomegalovirus (CMV) infection is common in the general population. CMV infection negatively affects disease course in transplant recipients and HIV patients. Whereas primary CMV infections may occur sporadically in seronegative patients, all seropositive patients with inflammatory bowel syndrome (IBD) are at risk for CMV reactivation due to the inflammatory mucosal and use of immunosuppressive medication. It is unclear whether latent CMV infection, and risk of reactivations, influences long-term disease outcomes. In this study, we aim to explore whether CMV infection affects disease outcomes in IBD patients. Methods: We performed a cross-sectional cohort study with 1404 patients with IBD from a single center. Clinical characteristics and disease outcomes were prospectively collected. We scrutinized CMV serology test results and performed additional CMV serology testing if serum was available. Results: Out of 699 IBD patients with CMV serology, 303 (43.3%) were seropositive, comparable to the general Dutch population. CMV seropositivity was associated with older age, longer IBD disease duration, non-Western origin, birth outside the Netherlands and a lower educational level ( Conclusions: CMV seropositivity does not influence disease outcomes of IBD patients and seems to be associated with a delay in IBD onset. Guidelines regarding CMV screening in patients with IBD are currently based on a low level of evidence. These data support the recommendation that routine CMV serology measurement is not necessary in the clinical care of IBD.
MeSH term(s)	Aged ; Cross-Sectional Studies ; Cytomegalovirus ; Cytomegalovirus Infections/complications ; HIV Infections ; Humans ; Inflammatory Bowel Diseases/complications ; Netherlands
Language	English
Publishing date	2020-07-07
Publishing country	England
Document type	Journal Article
ZDB-ID	82042-8
ISSN	1502-7708 ; 0036-5521
ISSN (online)	1502-7708
ISSN	0036-5521
DOI	10.1080/00365521.2020.1786853
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Article ; Online: Donor tobacco smoking is associated with postoperative thrombosis after primary liver transplantation.

Li, Yanni / Nieuwenhuis, Lianne M / Werner, Maureen J M / Voskuil, Michiel D / Gacesa, Ranko / Blokzijl, Hans / Lisman, Ton / Weersma, Rinse K / Porte, Robert J / Festen, Eleonora A M / de Meijer, Vincent E

Journal of thrombosis and haemostasis : JTH

2020 Volume 18, Issue 10, Page(s) 2590–2600

Abstract: Background: Thrombosis after liver transplantation is a leading cause of graft loss, morbidity, and mortality. Several known recipient- and surgery-related characteristics have been associated with increased risk of thrombosis after transplantation. ... ...

Abstract	Background: Thrombosis after liver transplantation is a leading cause of graft loss, morbidity, and mortality. Several known recipient- and surgery-related characteristics have been associated with increased risk of thrombosis after transplantation. Potential donor-related risk factors, however, remain largely undefined. Objectives: We aimed to identify risk factors for early post-transplantation thrombosis (<90 days) and to determine the impact of early postoperative thrombosis on long-term graft and patient survival. Patients/methods: A post hoc analysis was performed of an observational cohort study including all primary, adult liver transplantations performed between 1993 and 2018. Donor-, recipient-, and surgery-related characteristics were collected. Competing risk model analyses and multivariable regression analyses were performed to identify risk factors for developing early post-transplant thrombosis and graft failure. Results: From a total of 748 adult liver transplantations, 58 recipients (7.8%) developed a thrombosis after a median of 7 days. Post-transplantation thrombotic events included 25 hepatic artery thromboses, 13 portal vein thromboses, and 22 other thrombotic complications. Donor history of smoking was independently associated with early postoperative thrombosis (odds ratio [OR] 2.42; 95% confidence interval [CI], 1.29-4.52). Development of early post-transplant thrombosis was independently associated with patient mortality (hazard ratio [HR] 3.61; 95% CI 1.54-8.46) and graft failure (HR 5.80, 95% CI 3.26-10.33), respectively. Conclusion: Donor history of smoking conveys a more than two-fold increased risk of thrombosis after liver transplantation, independent of other factors. Post-transplant thrombosis was independently associated with decreased patient and graft survival.
MeSH term(s)	Adult ; Hepatic Artery ; Humans ; Liver Transplantation/adverse effects ; Postoperative Complications/epidemiology ; Retrospective Studies ; Risk Factors ; Thrombosis/epidemiology ; Thrombosis/etiology ; Tobacco Smoking
Language	English
Publishing date	2020-07-25
Publishing country	England
Document type	Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1111/jth.14983
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Zs.A 5805: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Predicted efficacy of a pharmacogenetic passport for inflammatory bowel disease.

Bangma, Amber / Voskuil, Michiel D / Uniken Venema, Werna T C / Brugge, Harm / Hu, Shixian / Lanting, Pauline / Franke, Lude / Dijkstra, Gerard / Festen, Eleonora A M / Weersma, Rinse K

Alimentary pharmacology & therapeutics

2020 Volume 51, Issue 11, Page(s) 1105–1115

Abstract: Background: High inter-individual variability in therapeutic response to drugs used in the management of Inflammatory Bowel Disease (IBD) leads to high morbidity and high costs. Genetic variants predictive of thiopurine-induced myelosuppression, ... ...

Abstract	Background: High inter-individual variability in therapeutic response to drugs used in the management of Inflammatory Bowel Disease (IBD) leads to high morbidity and high costs. Genetic variants predictive of thiopurine-induced myelosuppression, thiopurine-induced pancreatitis and immunogenicity of Tumour Necrosis Factor alpha (TNFα) antagonists have been identified, but uptake of pre-treatment pharmacogenetic testing into clinical guidelines has been slow. Aim: To explore the efficacy of a pharmacogenetic passport for IBD that includes multiple pharmacogenetic predictors of response. Methods: Patients with IBD exposed to thiopurines and/or TNFα antagonists were retrospectively evaluated for the presence of thiopurine toxicity and/or immunogenicity of TNFα antagonists. All patients were genotyped using both whole-exome sequencing and the Illumina Global Screening Array. An in-house-developed computational pipeline translated genetic data into an IBD pharmacogenetic passport that predicted risks for thiopurine toxicity and immunogenicity of TNFα antagonists per patient. Using pharmacogenetic-guided treatment guidelines, we calculated clinical efficacy estimates for pharmacogenetic testing for IBD. Results: Among 710 patients with IBD exposed to thiopurines and/or TNFα antagonists, 150 adverse drug responses occurred and our pharmacogenetic passport would have predicted 54 (36%) of these. Using a pharmacogenetic passport for IBD that includes genetic variants predictive of thiopurine-induced myelosuppression, thiopurine-induced pancreatitis, and immunogenicity of TNFα antagonists, 24 patients need to be genotyped to prevent one of these adverse drug responses. Conclusions: This study highlights the clinical efficacy of a pharmacogenetic passport for IBD. Implementation of such a pharmacogenetic passport into clinical management of IBD may contribute to a reduction in adverse drug responses.
MeSH term(s)	Adolescent ; Adult ; Aged ; Biomarkers, Pharmacological/analysis ; Case-Control Studies ; Female ; Genotype ; Humans ; Immunosuppressive Agents/therapeutic use ; Inflammatory Bowel Diseases/diagnosis ; Inflammatory Bowel Diseases/drug therapy ; Inflammatory Bowel Diseases/genetics ; Male ; Middle Aged ; Pharmacogenomic Testing/methods ; Pharmacogenomic Variants/genetics ; Predictive Value of Tests ; Prognosis ; Reproducibility of Results ; Retrospective Studies ; Transcriptome/drug effects ; Treatment Outcome ; Young Adult
Chemical Substances	Biomarkers, Pharmacological ; Immunosuppressive Agents
Language	English
Publishing date	2020-05-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639012-2
ISSN	1365-2036 ; 0269-2813 ; 0953-0673
ISSN (online)	1365-2036
ISSN	0269-2813 ; 0953-0673
DOI	10.1111/apt.15762
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Article ; Online: Inflammation status modulates the effect of host genetic variation on intestinal gene expression in inflammatory bowel disease.

Hu, Shixian / Uniken Venema, Werna T / Westra, Harm-Jan / Vich Vila, Arnau / Barbieri, Ruggero / Voskuil, Michiel D / Blokzijl, Tjasso / Jansen, Bernadien H / Li, Yanni / Daly, Mark J / Xavier, Ramnik J / Dijkstra, Gerard / Festen, Eleonora A / Weersma, Rinse K

Nature communications

2021 Volume 12, Issue 1, Page(s) 1122

Abstract: More than 240 genetic risk loci have been associated with inflammatory bowel disease (IBD), but little is known about how they contribute to disease development in involved tissue. Here, we hypothesized that host genetic variation affects gene expression ...

Abstract	More than 240 genetic risk loci have been associated with inflammatory bowel disease (IBD), but little is known about how they contribute to disease development in involved tissue. Here, we hypothesized that host genetic variation affects gene expression in an inflammation-dependent way, and investigated 299 snap-frozen intestinal biopsies from inflamed and non-inflamed mucosa from 171 IBD patients. RNA-sequencing was performed, and genotypes were determined using whole exome sequencing and genome wide genotyping. In total, 28,746 genes and 6,894,979 SNPs were included. Linear mixed models identified 8,881 independent intestinal cis-expression quantitative trait loci (cis-eQTLs) (FDR < 0.05) and interaction analysis revealed 190 inflammation-dependent intestinal cis-eQTLs (FDR < 0.05), including known IBD-risk genes and genes encoding immune-cell receptors and antibodies. The inflammation-dependent cis-eQTL SNPs (eSNPs) mainly interact with prevalence of immune cell types. Inflammation-dependent intestinal cis-eQTLs reveal genetic susceptibility under inflammatory conditions that can help identify the cell types involved in and the pathways underlying inflammation, knowledge that may guide future drug development and profile patients for precision medicine in IBD.
MeSH term(s)	Adult ; Cohort Studies ; Female ; Gene Expression Regulation ; Genetic Predisposition to Disease ; Genetic Variation ; Humans ; Inflammation/genetics ; Inflammatory Bowel Diseases/genetics ; Inflammatory Bowel Diseases/pathology ; Intestines/pathology ; Male ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci/genetics
Language	English
Publishing date	2021-02-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-21458-z
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