• 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

The role of serum in interleukin 1 production by human monocytes activated by endotoxins and their polysaccharide moieties.

作者信息

Cavaillon J M, Haeffner-Cavaillon N

出版信息

Immunol Lett. 1985;10(1):35-41. doi: 10.1016/0165-2478(85)90047-1.

DOI:10.1016/0165-2478(85)90047-1
PMID:2861158
Abstract

Lipopolysaccharides (LPS) as well as polysaccharide (PS) moieties of Bordetella pertussis and Neisseria meningitidis endotoxins induced in vitro interleukin 1 (IL 1) secretion by human monocytes as evaluated by the co-mitogenic assay on C3H/HeJ thymocytes. Because of the role of serum in the specific binding of endotoxins to monocytes mediated by the polysaccharide region [12], experiments were undertaken to study the effect of serum on IL 1 induction. Although the presence of serum is not necessary for the secretion of IL 1 by monocytes stimulated by LPS or PS, the addition of very small amounts of human serum (0.1-1.6%) to the cultures of human adherent cells potentiated the IL 1 secretion, without modifying the background values. Natural anti-B. pertussis antibodies present in the serum were not responsible for the observed phenomenon. Heating at 56 degrees C for 30 min did not alter the enhancing effect. The data presented suggest that the serum component(s) and the IL 1 inducers (LPS or PS) act in synergism by two different pathways since the two signals can be delivered sequentially.

摘要

相似文献

1
The role of serum in interleukin 1 production by human monocytes activated by endotoxins and their polysaccharide moieties.
Immunol Lett. 1985;10(1):35-41. doi: 10.1016/0165-2478(85)90047-1.
2
Interleukin 1 secretion by human monocytes stimulated by the isolated polysaccharide region of the Bordetella pertussis endotoxin.百日咳博德特氏菌内毒素的分离多糖区域刺激人单核细胞分泌白细胞介素1 。
Mol Immunol. 1984 May;21(5):389-95. doi: 10.1016/0161-5890(84)90036-1.
3
Inability of pyrogenic, purified Bordetella pertussis lipid A to induce interleukin-1 release by human monocytes.致热的、纯化的百日咳博德特氏菌脂多糖无法诱导人单核细胞释放白细胞介素-1。
Infect Immun. 1986 Nov;54(2):465-71. doi: 10.1128/iai.54.2.465-471.1986.
4
Polymyxin-B inhibition of LPS-induced interleukin-1 secretion by human monocytes is dependent upon the LPS origin.多粘菌素B对脂多糖诱导人单核细胞分泌白细胞介素-1的抑制作用取决于脂多糖的来源。
Mol Immunol. 1986 Sep;23(9):965-9. doi: 10.1016/0161-5890(86)90127-6.
5
Inhibition of activated nonresponder C3H/HeJ lymphocytes by lipopolysaccharide endotoxin.脂多糖内毒素对活化的无反应性C3H/HeJ淋巴细胞的抑制作用。
Infect Immun. 1988 Dec;56(12):3040-5. doi: 10.1128/iai.56.12.3040-3045.1988.
6
Inhibition by gangliosides of the specific binding of lipopolysaccharide (LPS) to human monocytes prevents LPS-induced interleukin-1 production.神经节苷脂对脂多糖(LPS)与人单核细胞特异性结合的抑制作用可防止LPS诱导的白细胞介素-1产生。
Cell Immunol. 1987 May;106(2):293-303. doi: 10.1016/0008-8749(87)90173-0.
7
Interleukin-1 induction by lipopolysaccharides: structural requirements of the 3-deoxy-D-manno-2-octulosonic acid (KDO).脂多糖诱导白细胞介素-1:3-脱氧-D-甘露糖-2-辛酮糖酸(KDO)的结构要求
Mol Immunol. 1989 May;26(5):485-94. doi: 10.1016/0161-5890(89)90108-9.
8
Specific binding of endotoxin to human monocytes and mouse macrophages: serum requirement.内毒素与人单核细胞和小鼠巨噬细胞的特异性结合:血清需求。
Cell Immunol. 1985 Mar;91(1):119-31. doi: 10.1016/0008-8749(85)90037-1.
9
Molecular requirement for interleukin 1 induction by lipopolysaccharide-stimulated human monocytes: involvement of the heptosyl-2-keto-3-deoxyoctulosonate region.脂多糖刺激的人单核细胞诱导白细胞介素-1的分子要求:庚糖基-2-酮-3-脱氧辛酮酸区域的参与
Eur J Immunol. 1986 Jan;16(1):87-91. doi: 10.1002/eji.1830160117.
10
Gram-negative bacteria induce proinflammatory cytokine production by monocytes in the absence of lipopolysaccharide (LPS).革兰氏阴性菌在缺乏脂多糖(LPS)的情况下可诱导单核细胞产生促炎细胞因子。
Clin Exp Immunol. 2000 Dec;122(3):312-5. doi: 10.1046/j.1365-2249.2000.01409.x.

引用本文的文献

1
From benzodiazepines to fatty acids and beyond: revisiting the role of ACBP/DBI.从苯二氮䓬类药物到脂肪酸类药物,以及更多:重新探讨 ACBP/DBI 的作用。
Trends Endocrinol Metab. 2021 Nov;32(11):890-903. doi: 10.1016/j.tem.2021.08.009. Epub 2021 Sep 23.
2
Metabolic and psychiatric effects of acyl coenzyme A binding protein (ACBP)/diazepam binding inhibitor (DBI).酰基辅酶A结合蛋白(ACBP)/地西泮结合抑制剂(DBI)的代谢和精神效应。
Cell Death Dis. 2020 Jul 6;11(7):502. doi: 10.1038/s41419-020-2716-5.
3
Inhibition of endotoxin-induced activation of human monocytes by human lipoproteins.
人脂蛋白对内毒素诱导的人单核细胞活化的抑制作用。
Infect Immun. 1989 Jul;57(7):2237-45. doi: 10.1128/iai.57.7.2237-2245.1989.
4
Dissociation of cell-associated interleukin-1 (IL-1) and IL-1 release induced by lipopolysaccharide and lipid A.脂多糖和脂质A诱导的细胞相关白细胞介素-1(IL-1)的解离及IL-1释放
Infect Immun. 1989 Mar;57(3):791-7. doi: 10.1128/iai.57.3.791-797.1989.
5
Enzymatically deacylated Neisseria lipopolysaccharide (LPS) inhibits murine splenocyte mitogenesis induced by LPS.酶促去酰化的奈瑟氏菌脂多糖(LPS)可抑制由LPS诱导的小鼠脾细胞有丝分裂。
Infect Immun. 1991 Jun;59(6):1881-7. doi: 10.1128/iai.59.6.1881-1887.1991.