The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Magali De Bruyn - One of the best experts on this subject based on the ideXlab platform.
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the ulcerative colitis response index for detection of mucosal healing in patients treated with anti tumour necrosis factor
Journal of Crohns & Colitis, 2020Co-Authors: Magali De Bruyn, Marc Ferrante, Ghislain Opdenakker, Gert Van Assche, Randy Ringold, Erik Martens, Avinoam Dukler, Severine VermeireAbstract:BACKGROUND Surrogate markers that accurately detect mucosal healing [MH] in patients with ulcerative colitis [UC] are urgently needed. Several stool neutrophil-related proteins are currently used as biomarkers for MH. However, the sensitivity and specificity are not sufficient to avoid unnecessary endoscopic evaluations. METHODS Novel serum neutrophil-related markers (neutrophil gelatinase B-associated lipocalin and matrix metalloproteinase-9 [NGAL-MMP-9 complex], cathelicidin LL-37 and chitinase 3-like 1 [CHI3L1]), together with C-reactive protein [CRP] and neutrophil counts were studied. Serum samples were obtained from 176 anti-tumour necrosis factor [anti-TNF]-treated UC patients (145 infliximab [IFX] and 31 adalimumab [ADM]) at baseline and after a median of 9.5 weeks. All patients had active disease prior to treatment (Mayo endoscopic subscore [MES] ≥ 2), and MH was defined as MES ≤ 1. Serum was also obtained from 75 healthy controls. Binary logistic regression analysis was used to generate the Ulcerative Colitis Response Index [UCRI]. The performance of individual markers and UCRI was tested with receiver operating characteristic analysis. RESULTS All neutrophil-related markers were significantly higher in active UC patients compared to healthy controls. In the IFX cohort, CRP, NGAL-MMP-9, CHI3L1 and neutrophil count decreased significantly after treatment and all marker levels were significantly lower in healers compared to non-healers following IFX. In the ADM cohort, CRP, NGAL-MMP-9, CHI3L1 and neutrophil count decreased significantly only in healers. UCRI [including CRP, CHI3L1, neutrophil count and LL-37] accurately detected MH in both IFX-treated (area under the curve [AUC] = 0.83) and ADM-treated [AUC = 0.79] patients. CONCLUSIONS The new UCRI index accurately detects MH after treatment with IFX and ADM. This panel is useful for monitoring MH in UC patients under anti-TNF treatment. PODCAST This article has an associated podcast which can be accessed at https://academic.oup.com/ecco-jcc/pages/podcast.
Henrik Vestergaard - One of the best experts on this subject based on the ideXlab platform.
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the association between genetic variations of CHI3L1 levels of the encoded glycoprotein ykl 40 and the lipid profile in a danish population
PLOS ONE, 2012Co-Authors: Stine Brinklov Thomsen, Camilla Noelle Rathcke, Henrik Vestergaard, Allan Linneberg, Tea SkaabyAbstract:Background: The inflammatory biomarker YKL-40 seems to play a role in atherosclerosis and is elevated in patients with obesity, cardiovascular disease and type 2 diabetes. Single nucleotide polymorphisms (SNPs) of the YKL-40 encoding gene, CHI3L1, are associated with inter-individual YKL-40 levels. One study has described an association between a promoter polymorphism of CHI3L1 and levels of low density lipoprotein. The objective of this study was to evaluate the influence of YKL-40 on lipid parameters by determining the association between polymorphisms of CHI3L1, serum YKL-40 and levels of the differentiated lipid profile in a Danish general population. Methodology/Principle Findings: 12 SNPs of CHI3L1 were genotyped, and serum YKL-40 and parameters of the lipid profile were measured in 2,656 Danes. Lipid profile and genotypes were available in another Danish population (n=6,784) for replication. Cholesterol and triglyceride levels increased with increasing YKL-40 quartile (both p,0.0001), and YKL-40 correlated with triglyceride levels (b=0.15, p,0.0001). Low density lipoprotein levels increased slightly from the 1 st to the 3 rd quartile (p=0.006). The highest YKL-40 quartile was associated with a greater risk of hypercholesterolemia compared to the lowest YKL-40 quartile (odds ratio 1.36, p=0.009). Minor homozygosity of rs12123883 was associated with higher triglyceride levels (p=0.022) and a higher prevalence of low high density lipoprotein (p=0.012), but these associations could not be confirmed in the replication population. Conclusions/Significance: Serum YKL-40 correlates with triglyceride levels in a representative group of the general Danish population. No consistent associations between SNPs of CHI3L1 and lipid levels could be documented.
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association of polymorphisms of the CHI3L1 gene with asthma and atopy a populations based study of 6514 danish adults
PLOS ONE, 2009Co-Authors: Camilla Noelle Rathcke, Johan Holmkvist, Lise Lotte N Husmoen, Torben Hansen, Oluf Pedersen, Henrik Vestergaard, Allan LinnebergAbstract:Background YKL-40 is a chitinase-like glycoprotein encoded by the chitinase 3-like 1 gene, CHI3L1, localized at chromosome 1q32.1. Increased levels of serum YKL-40 have been reported to be a biomarker for asthma and a reduced lung function. Interestingly, the C-allele of the -131 C-->G (rs4950928) polymorphism of CHI3L1 has been shown to associate with bronchial hyperresponsiveness and reduced lung function suggesting that variations in CHI3L1 may influence risk of asthma. The objective of the present study was to investigate the association of common variation in the CHI3L1 locus with asthma, atopy and lung function in a large population-based sample of adults. Methods/principal findings Eleven single nucleotide polymorphisms (SNPs) of CHI3L1 including rs4950928 were genotyped in 6514 individuals. Asthma was defined as self-reported history of physician-diagnosed asthma. Total IgE and specific IgE to inhalant allergens were measured on serum samples. Lung function was measured by spirometry. Homozygosity of the rs4950928 G allele as compared to homozygosity of the C allele was associated with self-reported physician diagnosed asthma (OR 1.5 (95% CI, 1.00-2.26)) and with prevalence of atopic asthma (OR 1.93 (95% CI, 1.21-3.07)) after adjustment for age, sex, smoking status, socio-economic class and BMI. Carriers of rs883125 G allele had a significantly lower prevalence of atopy (OR 0.82 (CI, 0.72; 0.94)) as compared to homozygosity of the C allele. None of the SNPs examined were significantly associated with FEV1. However, two SNPs (rs10399931 and rs4950930) appeared to be significantly associated with FEV(1)/FVC-ratio. Subgroup analyses of never-smokers did not consistently influence the associations in an either positively og negatively way. Conclusions In contrast to previous studies, the rs4950928 G allele, and not the C allele, was found to be associated with asthma. A few other SNPs of the CHI3L1 was found to be significantly associated with atopy and FEV1/FVC ratio, respectively. Thus, more studies seem warranted to establish the role of CHI3L1 gene in asthma and atopy.
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Variation in CHI3LI in relation to type 2 diabetes and related quantitative traits.
Public Library of Science (PLoS), 1Co-Authors: Camilla Noelle Rathcke, Johan Holmkvist, Torben Hansen, Torben Jørgensen, Knut Borch-johnsen, Oluf Borbye Pedersen, Henrik VestergaardAbstract:CHI3LI encoding the inflammatory glycoprotein YKL-40 is located on chromosome 1q32.1. YKL-40 is involved in inflammatory processes and patients with Type 2 Diabetes (T2D) have elevated circulating YKL-40 levels which correlate with their level of insulin resistance. Interestingly, it has been reported that rs10399931 (-329 G/A) of CHI3LI contributes to the inter-individual plasma YKL-40 levels in patients with sarcoidosis, and that rs4950928 (-131 C/G) is a susceptibility polymorphism for asthma and a decline in lung function. We hypothesized that single nucleotide polymorphisms (SNPs) or haplotypes thereof the CHI3LI locus might influence risk of T2D. The aim of the present study was to investigate the putative association between SNPs and haplotype blocks of CHI3LI and T2D and T2D related quantitative traits.Eleven SNPs of CHI3LI were genotyped in 6514 individuals from the Inter99 cohort and 2924 individuals from the outpatient clinic at Steno Diabetes Center. In cas-control studies a total of 2345 T2D patients and 5302 individuals with a normal glucose tolerance test were examined. We found no association between rs10399931 (OR, 0.98 (CI, 0.88-1.10), p = 0.76), rs4950928 (0.98 (0.87-1.10), p = 0.68) or any of the other SNPs with T2D. Similarly, we found no significant association between any of the 11 tgSNPs and T2D related quantitative traits, all p>0.14. None of the identified haplotype blocks of CHI3LI showed any association with T2D, all p>0.16.None of the examined SNPs or haplotype blocks of CHI3LI showed any association with T2D or T2D related quantitative traits. Estimates of insulin resistance and dysregulated glucose homeostasis in T2D do not seem to be accounted for by the examined variations of CHI3LI
Chun Geun Lee - One of the best experts on this subject based on the ideXlab platform.
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chitinase 3 like 1 drives allergic skin inflammation via th2 immunity and m2 macrophage activation
Clinical & Experimental Allergy, 2019Co-Authors: Eun Ji Kwak, Chun Geun Lee, Jung Yeon Hong, Mi Na Kim, Soo Yeon Kim, Seo Hyeong Kim, Chang Ook Park, Kyung Won Kim, Jack A EliasAbstract:Background Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by defective skin barrier and Th2 immune responses. Chitinase 3-like 1 (CHI3L1), also known as breast regression protein 39 (BRP-39) in mice and human homologue YKL-40, plays important roles in Th2 inflammation and allergen sensitization. CHI3L1 has been implicated in a variety of diseases including asthma characterized by inflammation, apoptosis and tissue remodelling, but its role in AD remains elusive. Objective The aim of this study was to investigate the role of CHI3L1 in the development and progression of AD. Results We investigated YKL-40 levels in the serum and skin of AD patients by ELISA and immunofluorescence, respectively. Using a murine model of AD induced by ovalbumin (OVA), we investigated Th2 immune responses, M2 macrophage activation and skin barrier gene expression using wild-type (WT) and BRP-39 null mutant (BRP-39-/- ) mice. YKL-40 level was significantly increased in serum of AD patients. In addition, both mRNA and protein expression levels of BRP-39 were higher in OVA-sensitized WT mice than in control mice. OVA-sensitized BRP-39-/- mice showed decreased epidermal thickness, lower total serum IgE, Th2 cytokine levels and CD4+ effector T cell populations than OVA-sensitized WT mice. Induction of BRP-39 was dominant in dermal macrophages. BRP-39 deficiency was found to be involved in M2 macrophage activation. Consistently, the YKL-40 level in the skin of AD patients was higher than in normal subjects and it was expressed in dermal macrophages. BRP-39 deficiency attenuated dysregulation of skin barrier and tight junction genes. Conclusions and clinical relevance These findings demonstrate that CHI3L1 mediates the development of AD induced by OVA, affecting Th2 inflammation, M2 macrophage activation and skin barrier function.
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galectin 3 interacts with the CHI3L1 axis and contributes to hermansky pudlak syndrome lung disease
Journal of Immunology, 2018Co-Authors: Yang Zhou, Daniel S Yang, Tung Nguyen, Yueming Cao, Suchitra Kamle, Changmin Lee, Bernadette R Gochuico, William A Gahl, Barry S Shea, Chun Geun LeeAbstract:Hermansky-Pudlak syndrome (HPS) comprises a group of inherited disorders caused by mutations that alter the function of lysosome-related organelles. Pulmonary fibrosis is the major cause of morbidity and mortality in HPS-1 and HPS-4 patients. However, the mechanisms that underlie the exaggerated injury and fibroproliferative repair responses in HPS have not been adequately defined. In particular, although Galectin-3 (Gal-3) is dysregulated in HPS, its roles in the pathogenesis of HPS have not been adequately defined. In addition, although chitinase 3-like 1 (CHI3L1) and its receptors play major roles in the injury and repair responses in HPS, the ability of Gal-3 to interact with or alter the function of these moieties has not been evaluated. In this article, we demonstrate that Gal-3 accumulates in exaggerated quantities in bronchoalveolar lavage fluids, and traffics abnormally and accumulates intracellularly in lung fibroblasts and macrophages from bleomycin-treated pale ear, HPS-1-deficient mice. We also demonstrate that Gal-3 drives epithelial apoptosis when in the extracellular space, and stimulates cell proliferation and myofibroblast differentiation when accumulated in fibroblasts and M2-like differentiation when accumulated in macrophages. Biophysical and signaling evaluations also demonstrated that Gal-3 physically interacts with IL-13Rα2 and CHI3L1, and competes with TMEM219 for IL-13Rα2 binding. By doing so, Gal-3 diminishes the antiapoptotic effects of and the antiapoptotic signaling induced by CHI3L1 in epithelial cells while augmenting macrophage Wnt/β-catenin signaling. Thus, Gal-3 contributes to the exaggerated injury and fibroproliferative repair responses in HPS by altering the antiapoptotic and fibroproliferative effects of CHI3L1 and its receptor complex in a tissue compartment-specific manner.
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chitinase 3 like 1 induces survival and proliferation of intestinal epithelial cells during chronic inflammation and colitis associated cancer by regulating s100a9
Oncotarget, 2015Co-Authors: Daren Low, Chun Geun Lee, Jack A Elias, Renuka Subramaniam, Li Lin, Tomoki Aomatsu, Atsushi Mizoguchi, Arianna K Degruttola, Akira Andoh, Mari MinokenudsonAbstract:Many host-factors are inducibly expressed during the development of inflammatory bowel disease (IBD), each having their unique properties, such as immune activation, bacterial clearance, and tissue repair/remodeling. Dysregulation/imbalance of these factors may have pathogenic effects that can contribute to colitis-associated cancer (CAC). Previous reports showed that IBD patients inducibly express colonic chitinase 3-like 1 (CHI3L1) that is further upregulated during CAC development. However, little is known about the direct pathogenic involvement of CHI3L1 in vivo. Here we demonstrate that CHI3L1 (aka Brp39) knockout (KO) mice treated with azoxymethane (AOM)/dextran sulphate sodium (DSS) developed severe colitis but lesser incidence of CAC as compared to that in wild-type (WT) mice. Highest CHI3L1 expression was found during the chronic phase of colitis, rather than the acute phase, and is essential to promote intestinal epithelial cell (IEC) proliferation in vivo. This CHI3L1-mediated cell proliferation/survival involves partial downregulation of the pro-apoptotic S100A9 protein that is highly expressed during the acute phase of colitis, by binding to the S100A9 receptor, RAGE (Receptor for Advanced Glycation End products). This interaction disrupts the S100A9-associated expression positive feedback loop during early immune activation, creating a CHI3L1hi S100A9low colonic environment, especially in the later phase of colitis, which promotes cell proliferation/survival of both normal IECs and tumor cells.
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abstract 3938 role of CHI3L1 ykl 40 in the tumor progression and metastasis in the lung
Cancer Research, 2013Co-Authors: Chun Geun Lee, Ja Seok Koo, Roy S Herbst, Jack A EliasAbstract:Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC The 18 glycosyl hydrolase gene family (GH18) contains chitinases and chitinase-like proteins (CLP) that lack enzyme activity. Chitinase 3-like-1 (CHI3L1; also called BRP-39 in mouse and YKL-40 in man), the prototypic CLP, is expressed in an exaggerated fashion in the serum and or tissues from patients with a variety of malignancies including breast, colon/rectum, ovary, melanoma, prostate, kidney, brain, bone, and lung. In many of these malignancies, there is a strong correlation between the levels of CHI3L1/YKL-40 and disease progression, prognosis and disease-free survival. However, the roles of YKL-40 in the development and progression of lung cancer has not been determined. To begin to address this issue, we generated CHI3L1/BRP-39 null mutant (CHI3L1-/-) and lung-specific overexpressing YKL-40 transgenic (YKL-40 Tg) mice and evaluated them in a number of settings. The studies demonstrated that CHI3L1/BRP-39/YKL-40 is an important regulator of cellular apoptosis, inflammation, angiogenesis and M2 macrophage differentiation. We also found that melanoma metastasis to the lung was significantly decreased in CHI3L1-/- mice and increased in YKL-40 Tg mice and that activation of the RIG-like helicase (RLH) innate immune pathway significantly decreased BRP-39 production and melanoma or breast cancer lung metastasis. Lastly, immunohistochemical (IHC) analysis demonstrated that, in mice with specific mutation of KRAS and/or p53, CHI3L1/BRP-39 is expressed in an exaggerated manner in normal peritumor tissues and lung cancer cells in early and late stages of lung cancer development, respectively. In combination, our preliminary studies demonstrate that CHI3L1/BRP-39/YKL-40 plays a critical role in the generation of a metastasis-permissive microenvironment and is dysregulated in the course of the development of primary lung cancers. Citation Format: Chun Geun Lee, Bing Ma, Ja Seok Koo, Roy S. Herbst, Jack A. Elias. Role of CHI3L1/YKL-40 in the tumor progression and metastasis in the lung. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3938. doi:10.1158/1538-7445.AM2013-3938
Jack A Elias - One of the best experts on this subject based on the ideXlab platform.
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chitinase 3 like 1 drives allergic skin inflammation via th2 immunity and m2 macrophage activation
Clinical & Experimental Allergy, 2019Co-Authors: Eun Ji Kwak, Chun Geun Lee, Jung Yeon Hong, Mi Na Kim, Soo Yeon Kim, Seo Hyeong Kim, Chang Ook Park, Kyung Won Kim, Jack A EliasAbstract:Background Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by defective skin barrier and Th2 immune responses. Chitinase 3-like 1 (CHI3L1), also known as breast regression protein 39 (BRP-39) in mice and human homologue YKL-40, plays important roles in Th2 inflammation and allergen sensitization. CHI3L1 has been implicated in a variety of diseases including asthma characterized by inflammation, apoptosis and tissue remodelling, but its role in AD remains elusive. Objective The aim of this study was to investigate the role of CHI3L1 in the development and progression of AD. Results We investigated YKL-40 levels in the serum and skin of AD patients by ELISA and immunofluorescence, respectively. Using a murine model of AD induced by ovalbumin (OVA), we investigated Th2 immune responses, M2 macrophage activation and skin barrier gene expression using wild-type (WT) and BRP-39 null mutant (BRP-39-/- ) mice. YKL-40 level was significantly increased in serum of AD patients. In addition, both mRNA and protein expression levels of BRP-39 were higher in OVA-sensitized WT mice than in control mice. OVA-sensitized BRP-39-/- mice showed decreased epidermal thickness, lower total serum IgE, Th2 cytokine levels and CD4+ effector T cell populations than OVA-sensitized WT mice. Induction of BRP-39 was dominant in dermal macrophages. BRP-39 deficiency was found to be involved in M2 macrophage activation. Consistently, the YKL-40 level in the skin of AD patients was higher than in normal subjects and it was expressed in dermal macrophages. BRP-39 deficiency attenuated dysregulation of skin barrier and tight junction genes. Conclusions and clinical relevance These findings demonstrate that CHI3L1 mediates the development of AD induced by OVA, affecting Th2 inflammation, M2 macrophage activation and skin barrier function.
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chitinase 3 like 1 induces survival and proliferation of intestinal epithelial cells during chronic inflammation and colitis associated cancer by regulating s100a9
Oncotarget, 2015Co-Authors: Daren Low, Chun Geun Lee, Jack A Elias, Renuka Subramaniam, Li Lin, Tomoki Aomatsu, Atsushi Mizoguchi, Arianna K Degruttola, Akira Andoh, Mari MinokenudsonAbstract:Many host-factors are inducibly expressed during the development of inflammatory bowel disease (IBD), each having their unique properties, such as immune activation, bacterial clearance, and tissue repair/remodeling. Dysregulation/imbalance of these factors may have pathogenic effects that can contribute to colitis-associated cancer (CAC). Previous reports showed that IBD patients inducibly express colonic chitinase 3-like 1 (CHI3L1) that is further upregulated during CAC development. However, little is known about the direct pathogenic involvement of CHI3L1 in vivo. Here we demonstrate that CHI3L1 (aka Brp39) knockout (KO) mice treated with azoxymethane (AOM)/dextran sulphate sodium (DSS) developed severe colitis but lesser incidence of CAC as compared to that in wild-type (WT) mice. Highest CHI3L1 expression was found during the chronic phase of colitis, rather than the acute phase, and is essential to promote intestinal epithelial cell (IEC) proliferation in vivo. This CHI3L1-mediated cell proliferation/survival involves partial downregulation of the pro-apoptotic S100A9 protein that is highly expressed during the acute phase of colitis, by binding to the S100A9 receptor, RAGE (Receptor for Advanced Glycation End products). This interaction disrupts the S100A9-associated expression positive feedback loop during early immune activation, creating a CHI3L1hi S100A9low colonic environment, especially in the later phase of colitis, which promotes cell proliferation/survival of both normal IECs and tumor cells.
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abstract 3938 role of CHI3L1 ykl 40 in the tumor progression and metastasis in the lung
Cancer Research, 2013Co-Authors: Chun Geun Lee, Ja Seok Koo, Roy S Herbst, Jack A EliasAbstract:Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC The 18 glycosyl hydrolase gene family (GH18) contains chitinases and chitinase-like proteins (CLP) that lack enzyme activity. Chitinase 3-like-1 (CHI3L1; also called BRP-39 in mouse and YKL-40 in man), the prototypic CLP, is expressed in an exaggerated fashion in the serum and or tissues from patients with a variety of malignancies including breast, colon/rectum, ovary, melanoma, prostate, kidney, brain, bone, and lung. In many of these malignancies, there is a strong correlation between the levels of CHI3L1/YKL-40 and disease progression, prognosis and disease-free survival. However, the roles of YKL-40 in the development and progression of lung cancer has not been determined. To begin to address this issue, we generated CHI3L1/BRP-39 null mutant (CHI3L1-/-) and lung-specific overexpressing YKL-40 transgenic (YKL-40 Tg) mice and evaluated them in a number of settings. The studies demonstrated that CHI3L1/BRP-39/YKL-40 is an important regulator of cellular apoptosis, inflammation, angiogenesis and M2 macrophage differentiation. We also found that melanoma metastasis to the lung was significantly decreased in CHI3L1-/- mice and increased in YKL-40 Tg mice and that activation of the RIG-like helicase (RLH) innate immune pathway significantly decreased BRP-39 production and melanoma or breast cancer lung metastasis. Lastly, immunohistochemical (IHC) analysis demonstrated that, in mice with specific mutation of KRAS and/or p53, CHI3L1/BRP-39 is expressed in an exaggerated manner in normal peritumor tissues and lung cancer cells in early and late stages of lung cancer development, respectively. In combination, our preliminary studies demonstrate that CHI3L1/BRP-39/YKL-40 plays a critical role in the generation of a metastasis-permissive microenvironment and is dysregulated in the course of the development of primary lung cancers. Citation Format: Chun Geun Lee, Bing Ma, Ja Seok Koo, Roy S. Herbst, Jack A. Elias. Role of CHI3L1/YKL-40 in the tumor progression and metastasis in the lung. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3938. doi:10.1158/1538-7445.AM2013-3938
Severine Vermeire - One of the best experts on this subject based on the ideXlab platform.
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the ulcerative colitis response index for detection of mucosal healing in patients treated with anti tumour necrosis factor
Journal of Crohns & Colitis, 2020Co-Authors: Magali De Bruyn, Marc Ferrante, Ghislain Opdenakker, Gert Van Assche, Randy Ringold, Erik Martens, Avinoam Dukler, Severine VermeireAbstract:BACKGROUND Surrogate markers that accurately detect mucosal healing [MH] in patients with ulcerative colitis [UC] are urgently needed. Several stool neutrophil-related proteins are currently used as biomarkers for MH. However, the sensitivity and specificity are not sufficient to avoid unnecessary endoscopic evaluations. METHODS Novel serum neutrophil-related markers (neutrophil gelatinase B-associated lipocalin and matrix metalloproteinase-9 [NGAL-MMP-9 complex], cathelicidin LL-37 and chitinase 3-like 1 [CHI3L1]), together with C-reactive protein [CRP] and neutrophil counts were studied. Serum samples were obtained from 176 anti-tumour necrosis factor [anti-TNF]-treated UC patients (145 infliximab [IFX] and 31 adalimumab [ADM]) at baseline and after a median of 9.5 weeks. All patients had active disease prior to treatment (Mayo endoscopic subscore [MES] ≥ 2), and MH was defined as MES ≤ 1. Serum was also obtained from 75 healthy controls. Binary logistic regression analysis was used to generate the Ulcerative Colitis Response Index [UCRI]. The performance of individual markers and UCRI was tested with receiver operating characteristic analysis. RESULTS All neutrophil-related markers were significantly higher in active UC patients compared to healthy controls. In the IFX cohort, CRP, NGAL-MMP-9, CHI3L1 and neutrophil count decreased significantly after treatment and all marker levels were significantly lower in healers compared to non-healers following IFX. In the ADM cohort, CRP, NGAL-MMP-9, CHI3L1 and neutrophil count decreased significantly only in healers. UCRI [including CRP, CHI3L1, neutrophil count and LL-37] accurately detected MH in both IFX-treated (area under the curve [AUC] = 0.83) and ADM-treated [AUC = 0.79] patients. CONCLUSIONS The new UCRI index accurately detects MH after treatment with IFX and ADM. This panel is useful for monitoring MH in UC patients under anti-TNF treatment. PODCAST This article has an associated podcast which can be accessed at https://academic.oup.com/ecco-jcc/pages/podcast.