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首页> 外文期刊>Infection and immunity >Deficient induction of the immune response to oral immunization with cholera toxin in malnourished rats during suckling.
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Deficient induction of the immune response to oral immunization with cholera toxin in malnourished rats during suckling.

机译：营养不良的哺乳期大鼠对霍乱毒素口服免疫的免疫反应诱导不足。

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Malnourished rats during suckling were orally immunized with cholera toxin (CT) after different periods of refeeding. Intestinal fluids, sera, and supernatant fluids from cultured mesenteric lymph node (MLN) cells were obtained after rats were given three doses of CT and analyzed by enzyme-linked immunosorbent assay (ELISA) to evaluate the specific antibody response. Serum-specific immunoglobulin G (IgG), IgA, and IgM were severely diminished in malnourished rats immunized with three doses of CT after 1 week of refeeding when compared with those of controls. Also, a decreased IgA ELISA titer of the intestinal fluids and abrogation of the capacity to neutralize the CT in the intestinal ligated loop test were found. When a booster was given at 113 days of age, the immune response continued to be affected in the serum and the intestinal fluid. The results from the analysis of the supernatant fluids from cultured MLN cells were coincident with those mentioned above. When one dose of CT was administered into Peyer's patches (PP) after 1 week of refeeding, an impaired immune response was found in the intestinal fluid of malnourished rats during suckling compared with that of controls. This result together with the analysis of supernatant from MLN and PP cell cultures suggests that antigen triggering in the PP was affected. When the refeeding period was extended to 30 days and then the first dose of CT was administered, the antibody immune responses in intestinal fluid serum and supernatant fluid approached control values. These observations reinforce the fact that the gut-associated lymphoid tissue immaturity of the rats when they received the first CT dose (at 28 days old) was the main reason for the decreased immune response observed in the experimental group.
机译：在哺乳期间营养不良的大鼠在不同的喂食期后口服霍乱毒素（CT）免疫。给大鼠给予三剂CT并通过酶联免疫吸附测定（ELISA）分析以评估特异性抗体反应后，从培养的肠系膜淋巴结（MLN）细胞获得肠液，血清和上清液。与对照组相比，在进食1周后用三剂CT免疫的营养不良的大鼠中，血清特异性免疫球蛋白G（IgG），IgA和IgM严重降低。另外，在肠结扎环试验中发现肠液的IgA ELISA滴度降低，中和CT的能力丧失。当在113日龄时加强免疫时，血清和肠液中的免疫反应继续受到影响。来自培养的MLN细胞的上清液的分析结果与上述结果一致。再喂食1周后，在Peyer's斑块（PP）中施用一剂CT时，与对照组相比，营养不良的大鼠肠内乳汁在免疫过程中发现免疫反应减弱。该结果以及对MLN和PP细胞培养上清液的分析表明，PP中的抗原触发受到影响。当再喂食期延长至30天，然后给予第一剂CT时，肠液血清和上清液中的抗体免疫反应达到对照值。这些观察结果加强了这样的事实，即在大鼠接受第一个CT剂量（28天大）时，它们的肠道相关淋巴样组织不成熟是在实验组中观察到免疫应答降低的主要原因。

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