小鼠非致命性疟疾感染对胶原蛋白诱导的关节炎的缓解不需要IL-10。

IF 1.5 4区 医学 Q3 PARASITOLOGY Parasitology International Pub Date : 2024-11-17 DOI:10.1016/j.parint.2024.102993
Shoichi Shimizu , Junko Shin , Takuma Ota , Hirofumi Kondo , Susumu Nakae , Katsuko Sudo , Eman M. Gaballah , Kentaro Morita , Yoshio Osada
{"title":"小鼠非致命性疟疾感染对胶原蛋白诱导的关节炎的缓解不需要IL-10。","authors":"Shoichi Shimizu ,&nbsp;Junko Shin ,&nbsp;Takuma Ota ,&nbsp;Hirofumi Kondo ,&nbsp;Susumu Nakae ,&nbsp;Katsuko Sudo ,&nbsp;Eman M. Gaballah ,&nbsp;Kentaro Morita ,&nbsp;Yoshio Osada","doi":"10.1016/j.parint.2024.102993","DOIUrl":null,"url":null,"abstract":"<div><div>We previously reported that <em>Plasmodium yoelii</em> 17XNL (Py), a non-lethal rodent malarial parasite, could suppress collagen-induced arthritis (CIA) and increase the production of T cell-derived interleukin (IL)-10. However, it remained unclear whether IL-10 is essential for the Py-induced suppression of CIA. Male IL-10 knockout (KO) DBA/1 J mice were immunized with bovine type II collagen (CII) and subsequently infected with Py at one week post-immunization. The development of arthritis was evaluated by an arthritis score up to 6 weeks post-immunization. At 3 weeks post-immunization, cytokine production from splenocytes and serum anti-CII IgG/IgG1/IgG2a levels were compared between non-infected control mice and Py-infected mice. Py infection inhibited the development of CIA in IL-10KO mice until 4 weeks post-immunization, after which the arthritis score reached levels comparable with the control mice. Both pro-arthritic (IL-17 and TNF-α) and anti-arthritic (IFN-γ and IL-4) cytokines were down-regulated during the periods of parasitemia, while no significant differences were observed in levels of anti-CII IgG antibodies. Our findings indicate that Py alleviates CIA via IL-10-independent mechanisms.</div></div>","PeriodicalId":19983,"journal":{"name":"Parasitology International","volume":"104 ","pages":"Article 102993"},"PeriodicalIF":1.5000,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"IL-10 is not required for the alleviation of collagen-induced arthritis by non-lethal malarial infection in mice\",\"authors\":\"Shoichi Shimizu ,&nbsp;Junko Shin ,&nbsp;Takuma Ota ,&nbsp;Hirofumi Kondo ,&nbsp;Susumu Nakae ,&nbsp;Katsuko Sudo ,&nbsp;Eman M. Gaballah ,&nbsp;Kentaro Morita ,&nbsp;Yoshio Osada\",\"doi\":\"10.1016/j.parint.2024.102993\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>We previously reported that <em>Plasmodium yoelii</em> 17XNL (Py), a non-lethal rodent malarial parasite, could suppress collagen-induced arthritis (CIA) and increase the production of T cell-derived interleukin (IL)-10. However, it remained unclear whether IL-10 is essential for the Py-induced suppression of CIA. Male IL-10 knockout (KO) DBA/1 J mice were immunized with bovine type II collagen (CII) and subsequently infected with Py at one week post-immunization. The development of arthritis was evaluated by an arthritis score up to 6 weeks post-immunization. At 3 weeks post-immunization, cytokine production from splenocytes and serum anti-CII IgG/IgG1/IgG2a levels were compared between non-infected control mice and Py-infected mice. Py infection inhibited the development of CIA in IL-10KO mice until 4 weeks post-immunization, after which the arthritis score reached levels comparable with the control mice. Both pro-arthritic (IL-17 and TNF-α) and anti-arthritic (IFN-γ and IL-4) cytokines were down-regulated during the periods of parasitemia, while no significant differences were observed in levels of anti-CII IgG antibodies. Our findings indicate that Py alleviates CIA via IL-10-independent mechanisms.</div></div>\",\"PeriodicalId\":19983,\"journal\":{\"name\":\"Parasitology International\",\"volume\":\"104 \",\"pages\":\"Article 102993\"},\"PeriodicalIF\":1.5000,\"publicationDate\":\"2024-11-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Parasitology International\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1383576924001442\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"PARASITOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Parasitology International","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1383576924001442","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PARASITOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

我们以前曾报道过疟原虫yoelii 17XNL(Py),一种非致命的啮齿类疟原虫,可以抑制胶原诱导的关节炎(CIA)并增加T细胞衍生的白细胞介素(IL)-10的产生。然而,IL-10对疟原虫诱导的CIA抑制作用是否必不可少仍不清楚。用牛Ⅱ型胶原蛋白(CII)免疫雄性IL-10基因敲除(KO)DBA/1 J小鼠,然后在免疫后一周用Py感染。免疫后 6 周内,通过关节炎评分来评估关节炎的发展情况。免疫后 3 周,比较未感染对照组小鼠和感染 Py 组小鼠脾细胞产生的细胞因子以及血清中抗 CII IgG/IgG1/IgG2a 的水平。Py感染抑制了IL-10KO小鼠CIA的发展,直到免疫后4周,其关节炎评分才达到与对照组小鼠相当的水平。在寄生虫血症期间,促关节炎细胞因子(IL-17 和 TNF-α)和抗关节炎细胞因子(IFN-γ 和 IL-4)都出现了下调,而抗 CII IgG 抗体的水平没有明显差异。我们的研究结果表明,Py 可通过与 IL-10 无关的机制缓解 CIA。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

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
IL-10 is not required for the alleviation of collagen-induced arthritis by non-lethal malarial infection in mice
We previously reported that Plasmodium yoelii 17XNL (Py), a non-lethal rodent malarial parasite, could suppress collagen-induced arthritis (CIA) and increase the production of T cell-derived interleukin (IL)-10. However, it remained unclear whether IL-10 is essential for the Py-induced suppression of CIA. Male IL-10 knockout (KO) DBA/1 J mice were immunized with bovine type II collagen (CII) and subsequently infected with Py at one week post-immunization. The development of arthritis was evaluated by an arthritis score up to 6 weeks post-immunization. At 3 weeks post-immunization, cytokine production from splenocytes and serum anti-CII IgG/IgG1/IgG2a levels were compared between non-infected control mice and Py-infected mice. Py infection inhibited the development of CIA in IL-10KO mice until 4 weeks post-immunization, after which the arthritis score reached levels comparable with the control mice. Both pro-arthritic (IL-17 and TNF-α) and anti-arthritic (IFN-γ and IL-4) cytokines were down-regulated during the periods of parasitemia, while no significant differences were observed in levels of anti-CII IgG antibodies. Our findings indicate that Py alleviates CIA via IL-10-independent mechanisms.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Parasitology International
Parasitology International 医学-寄生虫学
CiteScore
4.00
自引率
10.50%
发文量
140
审稿时长
61 days
期刊介绍: Parasitology International provides a medium for rapid, carefully reviewed publications in the field of human and animal parasitology. Original papers, rapid communications, and original case reports from all geographical areas and covering all parasitological disciplines, including structure, immunology, cell biology, biochemistry, molecular biology, and systematics, may be submitted. Reviews on recent developments are invited regularly, but suggestions in this respect are welcome. Letters to the Editor commenting on any aspect of the Journal are also welcome.
期刊最新文献
Epidemiology of Leishmaniasis: Risk factors for its pathology and infection Gnathostoma doloresi in domestic pigs in the Republic of Palau, 2020-2022. Parasitic helminths and protozoa: Treasure boxes of disease modifying anti-rheumatic drugs. A new focus of Taenia asiatica taeniasis in North Sumatra, Indonesia: Molecular confirmation and prevalence Dr. Jekyll and Mr. Hyde in sand fly saliva
×
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