Interleukin 17 B regulates colonic myeloid cell infiltration in a mouse model of DSS-induced colitis

Zhang, Xiaomin; Zhang, Xiaokai; Song, Xiaomei; Xiang, Chuanying; He, Canfei; Xie, Yuan; Zhou, Yangyang; Wang, Ning; Guo, Gang; Zhang, Weijun; Li, Yan; Liu, Kaiyun; Zou, Quanming; Guo, Hong; Shi, Yu

doi:10.3389/fimmu.2023.1055256

Cited by 8 publications

(5 citation statements)

References 31 publications

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“…However, there are few studies on IL-17B in IBD. One of the few existing studies suggested that IL-17B regulates the response of colonic myeloid cells to inhibit colitis ( 59 ), which is the same as the results of this study. IL-17A is generally considered to play a promoting role in NAFLD, while IL-17F has been reported to play a role in preventing liver function damage in NAFLD ( 60 ), which is also consistent with the results of this study.…”

Section: Discussionsupporting

confidence: 90%

Exploration of the core pathway of inflammatory bowel disease complicated with metabolic fatty liver and two-sample Mendelian randomization study of the causal relationships behind the disease

Wei,

Wang

2024

Front. Immunol.

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BackgroundInflammatory bowel disease (IBD) is often associated with complex extraintestinal manifestations. The incidence of nonalcoholic fatty liver disease (NAFLD) in IBD populations is increasing yearly. However, the mechanism of interaction between NAFLD and IBD is not clear. Consequently, this study aimed to explore the common genetic characteristics of IBD and NAFLD and identify potential therapeutic targets.Materials and methodsGene chip datasets for IBD and NAFLD were obtained from the Gene Expression Omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was performed to identify modules in those datasets related to IBD and NAFLD. ClueGO was used for biological analysis of the shared genes between IBD and NAFLD. Based on the Human MicroRNA Disease Database (HMDD), microRNAs (miRNAs) common to NAFLD and IBD were obtained. Potential target genes for the miRNAs were predicted using the miRTarbase, miRDB, and TargetScan databases. Two-sample Mendelian randomization (MR) and two-way MR were used to explore the causal relationship between Interleukin-17 (IL-17) and the risk of IBD and NAFLD using data from GWAS retrieved from an open database.ResultsThrough WGCNA, gene modules of interest were identified. GO enrichment analysis using ClueGO suggested that the abnormal secretion of chemokines may be a common pathophysiological feature of IBD and NAFLD, and that the IL-17-related pathway may be a common key pathway for the pathological changes that occur in IBD and NAFLD. The core differentially expressed genes (DEGs) in IBD and NAFLD were identified and included COL1A1, LUM, CCL22, CCL2, THBS2, COL1A2, MMP9, and CXCL8. Another cohort was used for validation. Finally, analysis of the miRNAs identified potential therapeutic targets. The MR results suggested that although there was no causal relationship between IBD and NAFLD, there were causal relationships between IL-17 and IBD and NAFLD.ConclusionWe established a comorbid model to explain the potential mechanism of IBD with NAFLD and identified the chemokine-related pathway mediated by cytokine IL-17 as the core pathway in IBD with NAFLD, in which miRNA also plays a role and thus provides potential therapeutic targets.

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Section: Discussionsupporting

confidence: 90%

Exploration of the core pathway of inflammatory bowel disease complicated with metabolic fatty liver and two-sample Mendelian randomization study of the causal relationships behind the disease

Wei,

Wang

2024

Front. Immunol.

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“…35 Damage to the intestinal mucosal barrier can result from increased leukocyte infiltration (CD45 positive cells) in the colon. 36 Our immunohistochemical results showed that the number of CD45 positive cells in the colon was significantly higher in the DSS-alone group as compared to that in the control group. The effect was significantly reduced after 2-week recovery.…”

Section: Resultsmentioning

confidence: 58%

d-Mannose promotes recovery from experimental colitis by inducing AMPK phosphorylation to stimulate epithelial repair

Zhang,

Zhao,

Gao

et al. 2024

Food Funct.

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“…To focus on the development of this methodology, we opted for IHC targets that have already been utilized in existing literature. We plan to introduce functional markers in future work, especially considering the growing application of single cell studies to mouse models of colitis 51 – 53 .…”

Section: Discussionmentioning

confidence: 99%

Computational immunohistochemical mapping adds immune context to histological phenotypes in mouse models of colitis

Kobayashi,

Sullivan,

Bialkowska

et al. 2023

Sci Rep

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Inflammatory bowel disease (IBD) is characterized by chronic, dysregulated inflammation in the gastrointestinal tract. The heterogeneity of IBD is reflected through two major subtypes, Crohn’s Disease (CD) and Ulcerative Colitis (UC). CD and UC differ across symptomatic presentation, histology, immune responses, and treatment. While colitis mouse models have been influential in deciphering IBD pathogenesis, no single model captures the full heterogeneity of clinical disease. The translational capacity of mouse models may be augmented by shifting to multi-mouse model studies that aggregate analysis across various well-controlled phenotypes. Here, we evaluate the value of histology in multi-mouse model characterizations by building upon a previous pipeline that detects histological disease classes in hematoxylin and eosin (H&E)-stained murine colons. Specifically, we map immune marker positivity across serially-sectioned slides to H&E histological classes across the dextran sodium sulfate (DSS) chemical induction model and the intestinal epithelium-specific, inducible Villin-CreERT2;Klf5fl/fl (Klf5ΔIND) genetic model. In this study, we construct the beginning frameworks to define H&E-patch-based immunophenotypes based on IHC-H&E mappings.

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Interleukin 17 B regulates colonic myeloid cell infiltration in a mouse model of DSS-induced colitis

Cited by 8 publications

References 31 publications

Exploration of the core pathway of inflammatory bowel disease complicated with metabolic fatty liver and two-sample Mendelian randomization study of the causal relationships behind the disease

Exploration of the core pathway of inflammatory bowel disease complicated with metabolic fatty liver and two-sample Mendelian randomization study of the causal relationships behind the disease

d-Mannose promotes recovery from experimental colitis by inducing AMPK phosphorylation to stimulate epithelial repair

Computational immunohistochemical mapping adds immune context to histological phenotypes in mouse models of colitis

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