Please use this identifier to cite or link to this item: https://doi.org/10.7150/thno.62046
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dc.titleMilk-derived extracellular vesicles alleviate ulcerative colitis by regulating the gut immunity and reshaping the microbiota
dc.contributor.authorTong, Lingjun
dc.contributor.authorHao, Haining
dc.contributor.authorZhang, Zhe
dc.contributor.authorLv, Youyou
dc.contributor.authorLiang, Xi
dc.contributor.authorLiu, Qiqi
dc.contributor.authorLiu, Tongjie
dc.contributor.authorGong, Pimin
dc.contributor.authorZhang, Lanwei
dc.contributor.authorCao, Fangfang
dc.contributor.authorPastorin, Giorgia
dc.contributor.authorLee, Chuen Neng
dc.contributor.authorChen, Xiaoyuan
dc.contributor.authorWang, Jiong-Wei
dc.contributor.authorYi, Huaxi
dc.date.accessioned2021-11-29T01:47:25Z
dc.date.available2021-11-29T01:47:25Z
dc.date.issued2021-01-01
dc.identifier.citationTong, Lingjun, Hao, Haining, Zhang, Zhe, Lv, Youyou, Liang, Xi, Liu, Qiqi, Liu, Tongjie, Gong, Pimin, Zhang, Lanwei, Cao, Fangfang, Pastorin, Giorgia, Lee, Chuen Neng, Chen, Xiaoyuan, Wang, Jiong-Wei, Yi, Huaxi (2021-01-01). Milk-derived extracellular vesicles alleviate ulcerative colitis by regulating the gut immunity and reshaping the microbiota. THERANOSTICS 11 (17) : 8570-8586. ScholarBank@NUS Repository. https://doi.org/10.7150/thno.62046
dc.identifier.issn18387640
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/208396
dc.description.abstractRationale: Bovine milk constitutes an essential part of human diet, especially for children, due to its enrichment of various nutrients. We recently developed an effective protocol for the isolation of extracellular vesicles from milk (mEVs) and discovered that mEVs contained large amounts of immune-active proteins and modulated the gut immunity and microbiota in healthy mice. Here, we aimed to explore the therapeutic effects of mEVs on inflammatory bowel disease. Methods: MicroRNAs and protein content in mEVs were analyzed by RNA sequencing and proteomics, respectively, followed by functional annotation. Ulcerative colitis (UC) was induced by feeding mice with dextran sulfate sodium. Intestinal immune cell populations were phenotyped by flow cytometry, and the gut microbiota was analyzed via 16S rRNA sequencing. Results: We showed that abundant proteins and microRNAs in mEVs were involved in the regulation of immune and inflammatory pathways and that oral administration of mEVs prevented colon shortening, reduced intestinal epithelium disruption, inhibited infiltration of inflammatory cells and tissue fibrosis in a mouse UC model. Mechanistically, mEVs attenuated inflammatory response via inhibiting TLR4-NF-κB signaling pathway and NLRP3 inflammasome activation. Furthermore, mEVs were able to correct cytokine production disorder and restore the balance between T helper type 17 (Th17) cells and interleukin-10+Foxp3+ regulatory T (Treg) cells in the inflamed colon. The disturbed gut microbiota in UC was also partially recovered upon treatment with mEVs. The correlation between the gut microbiota and cytokines suggests that mEVs may modulate intestinal immunity via influencing the gut microbiota. Conclusions: These findings reveal that mEVs alleviate colitis by regulating intestinal immune homeostasis via inhibiting TLR4-NF-κB and NLRP3 signaling pathways, restoring Treg/Th17 cell balance, and reshaping the gut microbiota.
dc.language.isoen
dc.publisherIVYSPRING INT PUBL
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectMedicine, Research & Experimental
dc.subjectResearch & Experimental Medicine
dc.subjectExtracellular vesicles
dc.subjectulcerative colitis
dc.subjectTreg/Th17 cell balance
dc.subjectintestinal immunity
dc.subjectgut microbiome
dc.subjectINTESTINAL INFLAMMATION
dc.subjectT-CELLS
dc.subjectRESPONSES
dc.subjectGROWTH
dc.subjectMICE
dc.subjectPROTECTS
dc.subjectEXOSOMES
dc.subjectBALANCE
dc.subjectCOLON
dc.subjectTLR4
dc.typeArticle
dc.date.updated2021-11-27T03:02:39Z
dc.contributor.departmentDEPT OF DIAGNOSTIC RADIOLOGY
dc.contributor.departmentDEPT OF PHARMACY
dc.contributor.departmentDEPT OF SURGERY
dc.description.doi10.7150/thno.62046
dc.description.sourcetitleTHERANOSTICS
dc.description.volume11
dc.description.issue17
dc.description.page8570-8586
dc.published.statePublished
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