Protein deficiency reduces natural antitumor immunity.

R Ruffmann, E Schlick, T Tartaris, W Budzynski, M A Chirigos
{"title":"Protein deficiency reduces natural antitumor immunity.","authors":"R Ruffmann,&nbsp;E Schlick,&nbsp;T Tartaris,&nbsp;W Budzynski,&nbsp;M A Chirigos","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Clinical data have shown that neoplastic diseases and/or related therapies frequently result in protein depletion of tumor-bearing patients. Depressions of acquired and specific immunity caused by protein depletion are well known. In an experimental model protein depletion was induced by lack of nutritional protein in otherwise isocaloric conditions in BALB/c and C57BL/6 mice over various time periods (max. 35 days). The results show that natural immune effector cells, natural killer cells, and monocyte/macrophages also during treatment with biological response modifiers (BRM) are depressed in their cytotoxic potentials in vitro and in vivo. Substantial and critical reductions of bone marrow cellularity (bone marrow nucleated cells) were also observed. In contrast, preliminary results show that if, following protein depletion, mice were treated parenterally with amino acids (Neo-aminomel, Boehringer-Ma. Co., FRG) complete restoration of immune parameters takes place. Adequate protein status is shown to be a crucial factor for natural immunity and therapy with BRM.</p>","PeriodicalId":77685,"journal":{"name":"Cancer detection and prevention. Supplement : official publication of the International Society for Preventive Oncology, Inc","volume":"1 ","pages":"15-27"},"PeriodicalIF":0.0000,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer detection and prevention. Supplement : official publication of the International Society for Preventive Oncology, Inc","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Clinical data have shown that neoplastic diseases and/or related therapies frequently result in protein depletion of tumor-bearing patients. Depressions of acquired and specific immunity caused by protein depletion are well known. In an experimental model protein depletion was induced by lack of nutritional protein in otherwise isocaloric conditions in BALB/c and C57BL/6 mice over various time periods (max. 35 days). The results show that natural immune effector cells, natural killer cells, and monocyte/macrophages also during treatment with biological response modifiers (BRM) are depressed in their cytotoxic potentials in vitro and in vivo. Substantial and critical reductions of bone marrow cellularity (bone marrow nucleated cells) were also observed. In contrast, preliminary results show that if, following protein depletion, mice were treated parenterally with amino acids (Neo-aminomel, Boehringer-Ma. Co., FRG) complete restoration of immune parameters takes place. Adequate protein status is shown to be a crucial factor for natural immunity and therapy with BRM.

蛋白质缺乏会降低天然的抗肿瘤免疫力。
临床资料显示,肿瘤疾病和/或相关治疗经常导致荷瘤患者的蛋白质耗竭。蛋白质耗竭引起的获得性和特异性免疫低下是众所周知的。在一个实验模型中,BALB/c和C57BL/6小鼠在不同的时间段内(最长时间)由于缺乏营养蛋白而导致蛋白质消耗。35天)。结果表明,自然免疫效应细胞、自然杀伤细胞和单核/巨噬细胞在体外和体内均受到生物反应修饰剂(biological response modifiers, BRM)抑制。骨髓细胞(骨髓有核细胞)的大量和临界减少也被观察到。相比之下,初步结果表明,如果在蛋白质耗尽后,小鼠被肠外注射氨基酸(新氨基氨基酸,勃林格-马。公司,FRG)免疫参数的完全恢复发生。充足的蛋白质状态被证明是自然免疫和BRM治疗的关键因素。
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
自引率
0.00%
发文量
0
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信