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PROTEIN MALNUTRITION & HELPER T CELL SUPPORT OF SIGA

蛋白质营养不良

基本信息

批准号：
3437661
负责人：
Thomas Martin Petro
金额：
$ 9.22万
依托单位：
UNIVERSITY OF NEBRASKA LINCOLN
依托单位国家：
美国
项目类别：
财政年份：
1989
资助国家：
美国
起止时间：
1989-04-01 至 1991-03-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/3437661
关键词：
Giardia Streptococcus mutans T lymphocyte bacterial disease dietary proteins enzyme linked immunosorbent assay immunotherapy interleukin 2 interleukin 4 interleukin 5 laboratory mouse leukocyte activation /transformation microorganism immunology nutrition related tag parasitic diseases protein deficiency secretory immune system tissue /cell culture

项目摘要

The major objective of the proposed research is to determine the etiology of the impaired secretory immunoglobulin (sIg) A production observed during dietary protein deficiency. This impairment likely contributes to the enhanced microbial infection or colonization of oral and mucosal surfaces during protein malnutrition. Total and antigen-specific secretory (S) IgA (following oral challenge with Giardia muris or Streptococcus mutans in saliva and intestinal secretions, using enzyme immunoassay (ETA), will be determine in mice fed 20% (20C) or 4% (4C) casein diets form weaning. The significance of sIgA reduction will be demonstrated by evaluating the ability of oral or intestinal pathogens to colonize at the respective surfaces. The hypthesis that dietary protein reductions reduces IgA by altering specific T cell subsets associated with help (H) (L3T4+) or suppression (S) (Lyt 2+), of the IgA immune response will be tested. Histological identification and quantification of T cell subsets in excised salivary glands, Peyer's patches, and spleen of mice fed 4C or 20C before and after infection will entail immunofluorescence using antibodies to L3T4 or Lyt2. Using the same antibodies, each subset will be isolated from dispersed tissues by "panning"; and the ability to generate IgA-enhancing factors will be evaluated before and during infection. L3T4+ T cell IgA enhancing lymphokines included, Interleukin 5 (IL5), IL4, IL2. Polyclonally stimulated T cell supernatants will be tested using EIA for the ability to promote IgA production, as opposed to IgG, IgG1 and IgM, production from purified B cells stimulated with lipopolysaccharide (LPS). Since IL4, IL5 could be generated by HT cell subsets distinct from IL2-generating HT cell subsets, the frequency of each subset in these tissues will be estimated using limiting dilution analysis. Noting the IgA-enhancing lymphokine which is impaired in mice fed 4C, attempts will be made to reconstitute the secretory IgA levels in mice fed 4C by treatment with the appropiate recombinant lymphokine. This research will contribute to understanding the problems of oral health in malnourished human populations as they relate to decreased secretory immunity and oral health.

拟议研究的主要目标是确定分泌型免疫球蛋白（sIg）A受损的病因学在膳食蛋白质缺乏期间观察到的生产。这损伤可能有助于增强微生物感染或在蛋白质降解过程中口腔和粘膜表面的定植营养不良总IgA和抗原特异性分泌型（S）伊加（经口攻毒后，唾液和肠分泌物中的变形菌，使用酶免疫测定法（ETA），将在喂食20%（20 ℃）或4% (4C)酪蛋白饮食形成断奶。 sIgA降低的意义将通过评估口语或肠道病原体在相应的表面上定殖。的假设饮食蛋白减少伊加改变与辅助相关的特异性T细胞亚群（H）（L3T4+）或抑制（S）（Lyt 2+），伊加免疫应答将被测试. T细胞的组织学鉴定和定量切除的唾液腺、派伊尔集合淋巴结和脾脏中的亚群在感染前后喂食4 ℃或20 ℃的小鼠将需要使用针对L3T4或Lyt2的抗体进行免疫荧光。使用相同的抗体，每个子集将从分散的通过“淘选”产生免疫球蛋白A增强的能力，将在感染前和感染过程中评估这些因素。 L3T4+ T 细胞伊加增强性淋巴因子包括白细胞介素5（IL 5），IL 4， IL 2。将检测多克隆刺激的T细胞上清液使用EIA促进伊加产生的能力，而不是 IgG、IgG1和IgM，由纯化的B细胞刺激产生脂多糖（LPS）。由于IL 4、IL 5可以由HT产生细胞亚群不同于产生IL 2的HT细胞亚群，将使用以下方法估计这些组织中每个子集的频率有限稀释分析注意到IgA增强淋巴因子在喂食4C的小鼠中受损，将尝试通过治疗重建喂食4C的小鼠中的分泌型伊加水平用合适的重组淋巴因子。这项研究将有助于了解口腔健康的问题，营养不良的人口，因为他们与减少分泌免疫和口腔健康。