The value of mRNA expression of S100A8 and S100A9 as blood-based biomarkers of inflammatory bowel disease

Kopi, Tayebeh Azramezani; Kadijani, Azade Amini; Parsian, Hadi; Shahrokh, Shabnam; Aghdaei, Hamid Asadzadeh; Mirzaei, Alireza; Balaii, Hedieh; Zali, Mohammad Reza

doi:10.1016/j.ajg.2019.07.002

Cited by 23 publications

(20 citation statements)

References 35 publications

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“…S100A9 is Ca 2+ binding protein belonging to the S100 family and an important pro-inflammatory mediator in acute and chronic inflammation. The S100A8 and S100A9 mRNA are differentially expressed in blood leucocytes of IBD patients compared to healthy control ( 19 ). Inhibition of S100A9 by a neutralizing anti-S100A9 antibody can reduce the colitis severity ( 20 ).…”

Section: Discussionmentioning

confidence: 99%

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

Zhang

Song

et al. 2023

Front. Immunol.

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Cytokines play vital roles in the pathogenesis of inflammatory bowel disease. IL17B is protective in the development of colitis. However, how IL17B regulates intestinal inflammation and what cells are regulated by IL17B is still unknown. Here, we aimed to illustrate the IL17B dependent cellular and molecular changes in colon tissue in a mouse colitis model. The results showed that IL17B expression in colon tissues was elevated in inflamed tissues than non-inflamed tissues of IBD patients. Wild type (WT) and Il17b deficient (Il17b-/-) mice were given 2.5% dextran sodium sulfate (DSS) water, and in some case, Il17b-/- mice were treated with recombinant mouse IL17B. IL17B deficiency resulted in severe DSS-induced colitis with exaggerated weight loss, shorter colon length, and elevated proinflammatory cytokines in colon. Reconstitution of Il17b-/- mice with recombinant IL17B alleviated the severity of DSS-induced colitis. Single cell transcriptional analyses of CD45+ immune cells in colonic lamina propria revealed that loss of IL17B resulted in an increased neutrophil infiltration and enhanced inflammatory cytokines in intestinal macrophages in colitis, which were confirmed by real-time PCR and flow cytometry. IL17B treatment also inhibited lipopolysaccharide-induced inflammation in bone marrow-derived macrophages and mice. IL17B inhibits colitis by regulating colonic myeloid cell response. It might represent a novel potential therapeutic approach to treat the colitis.

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Section: Discussionmentioning

confidence: 99%

“…Inhibition of S100A9 by a neutralizing anti-S100A9 antibody can reduce the colitis severity ( 20 ). Thus, S100A9 is a good biomarker and therapeutic target for colitis ( 19 , 21 ). In this study, S100A9 is exclusive expressed in neutrophils, suggesting it is also a good biomarker of neutrophils ( 19 , 21 ).…”

Section: Discussionmentioning

confidence: 99%

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

Zhang

Song

et al. 2023

Front. Immunol.

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“…Hence, CXCR2 is a potential target for UC treatment (Zhu et al, 2020). LCN2 (Østvik et al, 2013;Stallhofer et al, 2015;Buisson et al, 2018;Zollner et al, 2021) and S100A8 (Manolakis et al, 2011;Azramezani Kopi et al, 2019;Okada et al, 2019Okada et al, , 2020 are critical proinflammatory cytokines that have been reported in recent studies as potential molecular markers of UC in serum and stool samples. LCN2 and S100A8 also have antimicrobial effects and may be involved in the regulation of intestinal flora as antimicrobial peptides, which may be indirectly related to UC.…”

Section: Discussionmentioning

confidence: 99%

Integrated Analysis of Multiple Microarray Studies to Identify Novel Gene Signatures in Ulcerative Colitis

et al. 2021

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Background: Ulcerative colitis (UC) is a chronic, complicated, inflammatory disease with an increasing incidence and prevalence worldwide. However, the intrinsic molecular mechanisms underlying the pathogenesis of UC have not yet been fully elucidated.Methods: All UC datasets published in the GEO database were analyzed and summarized. Subsequently, the robust rank aggregation (RRA) method was used to identify differentially expressed genes (DEGs) between UC patients and controls. Gene functional annotation and PPI network analysis were performed to illustrate the potential functions of the DEGs. Some important functional modules from the protein-protein interaction (PPI) network were identified by molecular complex detection (MCODE), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG), and analyses were performed. The results of CytoHubba, a plug for integrated algorithm for biomolecular interaction networks combined with RRA analysis, were used to identify the hub genes. Finally, a mouse model of UC was established by dextran sulfate sodium salt (DSS) solution to verify the expression of hub genes.Results: A total of 6 datasets met the inclusion criteria (GSE38713, GSE59071, GSE73661, GSE75214, GSE87466, GSE92415). The RRA integrated analysis revealed 208 significant DEGs (132 upregulated genes and 76 downregulated genes). After constructing the PPI network by MCODE plug, modules with the top three scores were listed. The CytoHubba app and RRA identified six hub genes: LCN2, CXCL1, MMP3, IDO1, MMP1, and S100A8. We found through enrichment analysis that these functional modules and hub genes were mainly related to cytokine secretion, immune response, and cancer progression. With the mouse model, we found that the expression of all six hub genes in the UC group was higher than that in the control group (P < 0.05).Conclusion: The hub genes analyzed by the RRA method are highly reliable. These findings improve the understanding of the molecular mechanisms in UC pathogenesis.

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“…The expression of S100A9 varies between IBD patients and healthy controls, as well as between active and inactive illnesses. As a result, S100A9 was also used as a blood-based biomarker for IBD monitoring ( 51 ). S100A12 is a disease-specific marker, and higher fecal levels of S100A12 are observed in active IBD due to the disease’s abundant infiltrating neutrophils ( 52 ).…”

Section: Discussionmentioning

confidence: 99%

Identification and validation of the common pathogenesis and hub biomarkers in Hirschsprung disease complicated with Crohn’s disease

Wang

Xiao

et al. 2022

Front. Immunol.

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BackgroundAlthough increasing evidence has supported that Hirschsprung disease (HSCR) is the risk factor for children developing Crohn’s disease (CD), the common mechanism of its co-occurrence remains unknown. The purpose of this study is to further explore the underlying mechanism and biomarkers for the co-occurrence of HSCR and CD.MethodsThe Gene Expression Omnibus (GEO) database was used to obtain gene expression profiles for CD (GSE95095) and HSCR (GSE98502). Following the identification of the shared differentially expressed genes (DEGs) of CD and HSCR, functional annotation, protein–protein interaction (PPI) network creation, and module assembly were performed to discover hub genes. RT-qPCR was performed to validate the expression of the hub genes in HSCR samples. The receiver operating characteristic (ROC) curve was utilized to assess the accuracy of the hub genes as biomarkers in predicting CD in both the training dataset and test dataset.ResultsA total of 103 common DEGs (50 downregulated genes and 53 upregulated genes) were chosen for further investigation. The importance of chemokines and cytokines in these two disorders is highlighted by functional analysis. MCODE plug identified three important modules, which functionally enriched the immune system process. Finally, nine hub genes were identified using cytoHubba, including IL1B, IL10, CXCL10, ICAM1, EGR1, FCGR3A, S100A12, S100A9, and FPR1. The nine hub genes were mainly enriched in immune- and inflammation-related pathways. External data profiles and RT-qPCR confirmed the expression of the nine hub genes in HSCR and CD. ROC analysis revealed that the nine hub genes had a strong diagnostic value.ConclusionOur study reveals the common pathogenesis of HSCR and CD. These hub genes and diagnostic models may provide novel insight for the diagnosis and treatment of HSCR complicated with CD.

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The value of mRNA expression of S100A8 and S100A9 as blood-based biomarkers of inflammatory bowel disease

Cited by 23 publications

References 35 publications

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

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

Integrated Analysis of Multiple Microarray Studies to Identify Novel Gene Signatures in Ulcerative Colitis

Identification and validation of the common pathogenesis and hub biomarkers in Hirschsprung disease complicated with Crohn’s disease

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