Evaluation of TNF-α and IFN-γ primed conditioned medium of mesenchymal stem cell in acetic acid-induced mouse model of acute colitis

IF 3.7 4区医学 Q2 CELL BIOLOGY

Cellular immunology Pub Date : 2024-09-24 DOI:10.1016/j.cellimm.2024.104876

Manizhe Faghih , Mona Moshiri , Nader Mazrouei Arani , Fatemeh Ahmadzadeh , Narjes Jafari , Maryam Ghasemi , Saeid Abediankenari

{"title":"Evaluation of TNF-α and IFN-γ primed conditioned medium of mesenchymal stem cell in acetic acid-induced mouse model of acute colitis","authors":"Manizhe Faghih , Mona Moshiri , Nader Mazrouei Arani , Fatemeh Ahmadzadeh , Narjes Jafari , Maryam Ghasemi , Saeid Abediankenari","doi":"10.1016/j.cellimm.2024.104876","DOIUrl":null,"url":null,"abstract":"<div><div>IBD, an autoimmune-inflammatory disorder that affects people who are genetically prone to inflammation. There is a lot of interest in MSC-CM therapy, especially when primed with TNF-α + IFN-γ. Throughout the study, data were collected on the percentage of apoptotic cells, gene expression of ZO-1, Foxp3, GATA3, IDO-1, Muc2, <em>T</em>-bet, Notch1, TNFR2, and ROR-γt, colon weight and length, histopathological analysis, and DAI. TNF-α and IL-10 levels were assessed in addition to the NO level. The results suggest that primed MSC-CM improved DAI, mucosal deterioration, intestinal inflammation and NO concentration. The amount of TNF-α was decreased, but IL-10 and the colon’s percentage of apoptotic cells was increased. The mRNA expression of ZO-1, Foxp3, GATA3, IDO-1, and Muc2 genes increased greatly in the treatment groups, while the expression of <em>T</em>-bet, Notch1, TNFR2, and ROR-γt genes has decreased. These studies suggest that primed MSC-CM may combine with common treatments to improve responsiveness.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"405 ","pages":"Article 104876"},"PeriodicalIF":3.7000,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cellular immunology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0008874924000790","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

IBD, an autoimmune-inflammatory disorder that affects people who are genetically prone to inflammation. There is a lot of interest in MSC-CM therapy, especially when primed with TNF-α + IFN-γ. Throughout the study, data were collected on the percentage of apoptotic cells, gene expression of ZO-1, Foxp3, GATA3, IDO-1, Muc2, T-bet, Notch1, TNFR2, and ROR-γt, colon weight and length, histopathological analysis, and DAI. TNF-α and IL-10 levels were assessed in addition to the NO level. The results suggest that primed MSC-CM improved DAI, mucosal deterioration, intestinal inflammation and NO concentration. The amount of TNF-α was decreased, but IL-10 and the colon’s percentage of apoptotic cells was increased. The mRNA expression of ZO-1, Foxp3, GATA3, IDO-1, and Muc2 genes increased greatly in the treatment groups, while the expression of T-bet, Notch1, TNFR2, and ROR-γt genes has decreased. These studies suggest that primed MSC-CM may combine with common treatments to improve responsiveness.

查看原文本刊更多论文

间充质干细胞TNF-α和IFN-γ条件培养基在醋酸诱导的急性结肠炎小鼠模型中的应用评估

肠易激综合征是一种自身免疫炎症性疾病，易发于遗传性炎症患者。间充质干细胞-间充质干细胞疗法备受关注，尤其是在使用 TNF-α + IFN-γ 的情况下。在整个研究过程中，我们收集了凋亡细胞的百分比、ZO-1、Foxp3、GATA3、IDO-1、Muc2、T-bet、Notch1、TNFR2 和 ROR-γt 的基因表达、结肠重量和长度、组织病理学分析和 DAI 等数据。除 NO 水平外，还评估了 TNF-α 和 IL-10 水平。结果表明，间充质干细胞-CM能改善DAI、粘膜恶化、肠道炎症和NO浓度。TNF-α的含量降低了，但IL-10和结肠凋亡细胞的百分比增加了。治疗组中 ZO-1、Foxp3、GATA3、IDO-1 和 Muc2 基因的 mRNA 表达量大幅增加，而 T-bet、Notch1、TNFR2 和 ROR-γt 基因的表达量减少。这些研究表明，引诱间充质干细胞-间充质干细胞可与普通治疗方法相结合，提高反应性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Cellular immunology 生物-免疫学

CiteScore

8.20

自引率

2.30%

发文量

102

审稿时长

30 days

期刊介绍： Cellular Immunology publishes original investigations concerned with the immunological activities of cells in experimental or clinical situations. The scope of the journal encompasses the broad area of in vitro and in vivo studies of cellular immune responses. Purely clinical descriptive studies are not considered. Research Areas include: • Antigen receptor sites • Autoimmunity • Delayed-type hypersensitivity or cellular immunity • Immunologic deficiency states and their reconstitution • Immunologic surveillance and tumor immunity • Immunomodulation • Immunotherapy • Lymphokines and cytokines • Nonantibody immunity • Parasite immunology • Resistance to intracellular microbial and viral infection • Thymus and lymphocyte immunobiology • Transplantation immunology • Tumor immunity.