Serum IgA augments adhesiveness of cultured lung microvascular endothelial cells and suppresses angiogenesis

IF 3.7 4区 医学 Q2 CELL BIOLOGY Cellular immunology Pub Date : 2023-09-16 DOI:10.1016/j.cellimm.2023.104769
Kazufumi Takada , Maho Suzukawa , Sayaka Igarashi , Yuuki Uehara , Shizuka Watanabe , Sahoko Imoto , Masaki Ishii , Yoshiteru Morio , Hirotoshi Matsui , Masahiro Akishita , Ken Ohta
{"title":"Serum IgA augments adhesiveness of cultured lung microvascular endothelial cells and suppresses angiogenesis","authors":"Kazufumi Takada ,&nbsp;Maho Suzukawa ,&nbsp;Sayaka Igarashi ,&nbsp;Yuuki Uehara ,&nbsp;Shizuka Watanabe ,&nbsp;Sahoko Imoto ,&nbsp;Masaki Ishii ,&nbsp;Yoshiteru Morio ,&nbsp;Hirotoshi Matsui ,&nbsp;Masahiro Akishita ,&nbsp;Ken Ohta","doi":"10.1016/j.cellimm.2023.104769","DOIUrl":null,"url":null,"abstract":"<div><p>Immunoglobulin A (IgA) is important in local immunity and is also abundant in the blood. This study aimed to evaluate the effects of serum IgA on cultured lung microvascular endothelial cells (HMVEC-Ls), which are involved in the pathogenesis of inflammatory lung diseases. Serum IgA induced adhesion molecules and inflammatory cytokine production from HMVEC-Ls, and enhanced adhesion of peripheral blood mononuclear cells to HMVEC-Ls. In contrast, migration, proliferation, and tube formation of HMVEC-Ls were significantly suppressed by serum IgA. Experiments with siRNAs and western blotting revealed that two known IgA receptors, β1,4-galactosyltransferase 1 (b4GALT1) and asialoglycoprotein receptor 1 (ASGR1), and mitogen-activated protein kinase and nuclear factor-kappa B pathways were partly involved in serum IgA-induced cytokine production by HMVEC-Ls. Collectively, serum IgA enhanced cytokine production and adhesiveness of HMVEC-L, with b4GALT1 and ASGR1 partially being involved, and suppressed angiogenesis. Thus, serum IgA may be targeted to treat inflammatory lung diseases.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"393 ","pages":"Article 104769"},"PeriodicalIF":3.7000,"publicationDate":"2023-09-16","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/S0008874923001089","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

Immunoglobulin A (IgA) is important in local immunity and is also abundant in the blood. This study aimed to evaluate the effects of serum IgA on cultured lung microvascular endothelial cells (HMVEC-Ls), which are involved in the pathogenesis of inflammatory lung diseases. Serum IgA induced adhesion molecules and inflammatory cytokine production from HMVEC-Ls, and enhanced adhesion of peripheral blood mononuclear cells to HMVEC-Ls. In contrast, migration, proliferation, and tube formation of HMVEC-Ls were significantly suppressed by serum IgA. Experiments with siRNAs and western blotting revealed that two known IgA receptors, β1,4-galactosyltransferase 1 (b4GALT1) and asialoglycoprotein receptor 1 (ASGR1), and mitogen-activated protein kinase and nuclear factor-kappa B pathways were partly involved in serum IgA-induced cytokine production by HMVEC-Ls. Collectively, serum IgA enhanced cytokine production and adhesiveness of HMVEC-L, with b4GALT1 and ASGR1 partially being involved, and suppressed angiogenesis. Thus, serum IgA may be targeted to treat inflammatory lung diseases.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
血清IgA增强培养的肺微血管内皮细胞的粘附性并抑制血管生成。
免疫球蛋白A(IgA)在局部免疫中很重要,在血液中也很丰富。本研究旨在评估血清IgA对培养的肺微血管内皮细胞(HMVEC Ls)的影响,这些细胞参与了炎症性肺部疾病的发病机制。血清IgA诱导HMVEC Ls产生粘附分子和炎性细胞因子,并增强外周血单核细胞与HMVEC L的粘附。相反,血清IgA显著抑制HMVEC Ls的迁移、增殖和管形成。siRNA和蛋白质印迹实验表明,两种已知的IgA受体,β1,4-半乳糖基转移酶1(b4GALT1)和去唾液酸糖蛋白受体1(ASGR1),以及促分裂原活化蛋白激酶和核因子κB途径,部分参与了HMVEC Ls产生血清IgA诱导的细胞因子。总的来说,血清IgA增强了细胞因子的产生和HMVEC-L的粘附性,b4GALT1和ASGR1部分参与其中,并抑制了血管生成。因此,血清IgA可以靶向治疗炎症性肺部疾病。
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 去求助
来源期刊
Cellular immunology
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.
期刊最新文献
The CCL5/CCR5 axis in ulcerative colitis Immunomodulation by galectin-9: Distinct role in T cell populations, current therapeutic avenues and future potential Ubiquitination and degradation of MHC-II by Tim-3 inhibits antiviral immunity Gastrodenol suppresses NLRP3/GSDMD mediated pyroptosis and ameliorates inflammatory diseases Complement system component 3 deficiency modulates the phenotypic profile of murine macrophages
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1