• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

早期γ干扰素产生在痤疮丙酸杆菌诱导的小鼠对刚地弓形虫感染抗性中的重要性。

Importance of early gamma interferon production in Propionibacterium acnes-induced resistance to Toxoplasma gondii infection in mice.

作者信息

Shirahata T, Shimoi A, Kanda H, Goto H, Nakane A

机构信息

Department of Veterinary Microbiology, Obihiro University of Agriculture and Veterinary Medicine, Hokkaido, Japan.

出版信息

J Vet Med Sci. 1994 Apr;56(2):293-7. doi: 10.1292/jvms.56.293.

DOI:10.1292/jvms.56.293
PMID:8075217
Abstract

Treatment of mice with heat-killed Propionibacterium (P.) acnes conferred transient protection against Toxoplasma infection. To investigate the mechanism of this nonspecific resistance, the production of gamma interferon (IFN-gamma) by P. acnes-injected mice was evaluated in comparison with that by noninjected controls upon infection with Toxoplasma. Mice pretreated with this bacterium produced significantly more IFN-gamma than that produced by control mice up to 24 hr of infection. A single injection of anti-IFN-gamma MAb on day 0 but not later than day 3 of infection resulted in a total abrogation of the resistance conferred by P. acnes. Likewise, daily injection of cyclosporin A (Cs-A), a potent inhibitor of T cell function, during the first 3 days of Toxoplasma infection severely exacerbated the infection, in accordance with a marked suppression of the early IFN-gamma production. In contrast, the administration of Cs-A for 3 consecutive days starting at day 4 had no significant consequence on P. acnes-induced anti-toxoplasma resistance, while it reduced greatly the ability of P. acnes-injected mice to produce IFN-gamma in the later phase of infection. Moreover, no significant increase in mortality and suppression of IFN-gamma production was noted in mice receiving anti-asialo GM1 antibody. These results suggest that the early IFN-gamma production by T cells is an essential event for the establishment of P. acnes-induced anti-toxoplasma resistance in mice.

摘要

用热灭活痤疮丙酸杆菌处理小鼠可使其获得针对弓形虫感染的短暂保护。为了研究这种非特异性抗性的机制,在感染弓形虫后,评估了注射痤疮丙酸杆菌的小鼠与未注射的对照小鼠相比γ干扰素(IFN-γ)的产生情况。用这种细菌预处理的小鼠在感染后24小时内产生的IFN-γ明显多于对照小鼠。在感染第0天但不迟于第3天单次注射抗IFN-γ单克隆抗体导致痤疮丙酸杆菌所赋予的抗性完全丧失。同样,在弓形虫感染的前3天每天注射环孢素A(Cs-A),一种强效的T细胞功能抑制剂,会严重加剧感染,这与早期IFN-γ产生的显著抑制一致。相反,从第4天开始连续3天给予Cs-A对痤疮丙酸杆菌诱导的抗弓形虫抗性没有显著影响,而它大大降低了注射痤疮丙酸杆菌的小鼠在感染后期产生IFN-γ的能力。此外,接受抗去唾液酸GM1抗体的小鼠死亡率没有显著增加,IFN-γ产生也没有受到抑制。这些结果表明,T细胞早期产生IFN-γ是小鼠建立痤疮丙酸杆菌诱导的抗弓形虫抗性的关键事件。

相似文献

1
Importance of early gamma interferon production in Propionibacterium acnes-induced resistance to Toxoplasma gondii infection in mice.早期γ干扰素产生在痤疮丙酸杆菌诱导的小鼠对刚地弓形虫感染抗性中的重要性。
J Vet Med Sci. 1994 Apr;56(2):293-7. doi: 10.1292/jvms.56.293.
2
CD8+ T lymphocytes are the major cell population involved in the early gamma interferon response and resistance to acute primary Toxoplasma gondii infection in mice.CD8 + T淋巴细胞是参与小鼠早期γ干扰素反应及对急性原发性弓形虫感染抵抗力的主要细胞群体。
Microbiol Immunol. 1994;38(10):789-96. doi: 10.1111/j.1348-0421.1994.tb01858.x.
3
Protection against lethal toxoplasmosis in mice by an avirulent strain of Toxoplasma gondii: stimulation of IFN-gamma and TNF-alpha response.无毒力株刚地弓形虫对小鼠致死性弓形虫病的保护作用:IFN-γ和TNF-α反应的刺激
Exp Parasitol. 1999 Dec;93(4):231-40. doi: 10.1006/expr.1999.4457.
4
Induction of murine gamma interferon production by lipopolysaccharide and interleukin-2 in Propionibacterium acnes-induced peritoneal exudate cells.痤疮丙酸杆菌诱导的腹膜渗出细胞中脂多糖和白细胞介素-2对小鼠γ干扰素产生的诱导作用
Infect Immun. 1987 Feb;55(2):335-41. doi: 10.1128/iai.55.2.335-341.1987.
5
Effects of cyclosporin A on susceptibility and interferon-generating capacity in mice infected with Toxoplasma gondii.环孢素A对感染刚地弓形虫小鼠的易感性和干扰素生成能力的影响。
Nihon Juigaku Zasshi. 1990 Apr;52(2):387-93. doi: 10.1292/jvms1939.52.387.
6
A pivotal role of IL-12 in Th1-dependent mouse liver injury.白细胞介素-12在Th1依赖性小鼠肝损伤中起关键作用。
Int Immunol. 1996 Apr;8(4):569-76. doi: 10.1093/intimm/8.4.569.
7
Identification of STAT4-dependent and independent mechanisms of resistance to Toxoplasma gondii.对弓形虫耐药的STAT4依赖性和非依赖性机制的鉴定。
J Immunol. 2000 Sep 1;165(5):2619-27. doi: 10.4049/jimmunol.165.5.2619.
8
Gamma interferon mediates Propionibacterium acnes-induced hypersensitivity to lipopolysaccharide in mice.γ干扰素介导痤疮丙酸杆菌诱导的小鼠对脂多糖的超敏反应。
Infect Immun. 1992 May;60(5):1994-2001. doi: 10.1128/iai.60.5.1994-2001.1992.
9
Kinetics of interferon gamma production in vivo during infection with the S48 vaccine strain of Toxoplasma gondii.感染刚地弓形虫S48疫苗株期间体内γ干扰素产生的动力学
J Comp Pathol. 1995 Jul;113(1):89-94. doi: 10.1016/s0021-9975(05)80074-x.
10
Transforming growth factor-beta inhibits interleukin-12-induced production of interferon-gamma by natural killer cells: a role for transforming growth factor-beta in the regulation of T cell-independent resistance to Toxoplasma gondii.转化生长因子-β抑制自然杀伤细胞由白细胞介素-12诱导产生的γ干扰素:转化生长因子-β在调节对刚地弓形虫的非T细胞依赖性抗性中的作用。
Eur J Immunol. 1995 Apr;25(4):994-1000. doi: 10.1002/eji.1830250420.

引用本文的文献

1
Natural Killer cell-dependent and non-dependent anti-viral activity of 2-Cys Peroxiredoxin against HIV.2-半胱氨酸过氧化物酶对HIV的自然杀伤细胞依赖性和非依赖性抗病毒活性。
Int Trends Immun. 2013 Oct;1(4):69-77.
2
Regulatory T cells suppress natural killer cells during plasmid DNA vaccination in mice, blunting the CD8+ T cell immune response by the cytokine TGFbeta.调节性 T 细胞在小鼠的质粒 DNA 疫苗接种过程中抑制自然杀伤细胞,通过细胞因子 TGFbeta 使 CD8+T 细胞免疫反应迟钝。
PLoS One. 2010 Aug 19;5(8):e12281. doi: 10.1371/journal.pone.0012281.
3
Non-classical natural killer T cells modulate plasmid DNA vaccine antigen expression and vaccine-elicited immune responses by MCP-1 secretion after interaction with a beta2-microglobulin-independent CD1d.
非经典自然杀伤T细胞在与β2-微球蛋白非依赖性CD1d相互作用后,通过分泌单核细胞趋化蛋白-1调节质粒DNA疫苗的抗原表达和疫苗引发的免疫反应。
J Biol Chem. 2009 Dec 4;284(49):33800-6. doi: 10.1074/jbc.M109.019638. Epub 2009 Oct 15.