Differential gene expression during recall of behaviorally conditioned immune enhancement in rats: a pilot study.

Q2 Pharmacology, Toxicology and Pharmaceutics
F1000Research Pub Date : 2025-01-10 eCollection Date: 2022-01-01 DOI:10.12688/f1000research.123975.1
Markus Rueckels, Marcus Picard-Mareau
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引用次数: 0

Abstract

Background: Behaviorally conditioned immune functions are suggested to be regulated by bidirectional interactions between CNS and peripheral immune system via the hypothalamic-pituitary-adrenal (HPA) axis, sympathetic nervous system (SNS), and the parasympathetic nervous system (PNS). Since the current knowledge about biochemical pathways triggering conditioned immune enhancement is limited, the aim of this pilot study was gaining more insights into that.

Methods: Rats were conditioned with camphor smell and poly I:C injection, mimicking a viral infection. Following stimulus re-exposure, animals were sacrificed at different time points, and neural tissues along the HPA axis was analyzed with a rat genome array together with plasma protein using Luminex analysis.

Results: In the hypothalamus, we observed a strong upregulation of genes related to Wnt/β-catenin signaling (Otx2, Spp1, Fzd6, Zic1), monoaminergic transporter Slc18a2 and opioid-inhibitory G-protein Gpr88 as well as downregulation of dopaminergic receptors, vasoactive intestinal peptide Vip, and pro-melanin-concentrating hormone Pmch. In the pituitary, we recognized mostly upregulation of steroid synthesis in combination with GABAergic, cholinergic and opioid related neurotransmission, in adrenal glands, altered genes showed a pattern of activated metabolism plus upregulation of adrenoceptors Adrb3 and Adra1a. Data obtained from spleen showed a strong upregulation of immunomodulatory genes, chemo-/cytokines and glutamatergic/cholinergic neurotransmission related genes, as also confirmed by increased chemokine and ACTH levels in plasma.

Conclusions: Our data indicate that in addition to the classic HPA axis, there could be additional pathways as e.g. the cholinergic anti-inflammatory pathway (CAIP), connecting brain and immune system, modulating and finetuning communication between brain and immune system.

大鼠行为条件免疫增强记忆过程中的差异基因表达:一项初步研究
背景:行为条件免疫功能被认为是由中枢神经系统和外周免疫系统通过下丘脑-垂体-肾上腺(HPA)轴、交感神经系统(SNS)和副交感神经系统(PNS)双向相互作用调节的。由于目前对触发条件免疫增强的生化途径的了解有限,因此这项初步研究的目的是获得更多的见解。方法:大鼠用樟脑气味和聚I:C注射模拟病毒感染。刺激再暴露后,在不同时间点处死动物,用大鼠基因组阵列分析沿HPA轴的神经组织,用Luminex分析血浆蛋白。结果:下丘脑Wnt/β-catenin信号通路相关基因Otx2、Spp1、Fzd6、Zic1、单胺转运蛋白Slc18a2、阿片抑制g蛋白Gpr88表达明显上调,多巴胺能受体、血管活性肠肽Vip、促黑色素浓缩激素Pmch表达下调。在垂体中,我们认识到类固醇合成的上调主要与gaba能、胆碱能和阿片相关的神经传递相结合,在肾上腺中,改变的基因表现为代谢激活和肾上腺素受体Adrb3和Adra1a的上调。从脾脏获得的数据显示免疫调节基因、化学/细胞因子和谷氨酸/胆碱能神经传递相关基因的强烈上调,血浆趋化因子和ACTH水平升高也证实了这一点。结论:我们的数据表明,除了经典的HPA轴外,可能还有其他途径,如胆碱能抗炎途径(CAIP),连接大脑和免疫系统,调节和微调大脑和免疫系统之间的通信。
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来源期刊
F1000Research
F1000Research Pharmacology, Toxicology and Pharmaceutics-Pharmacology, Toxicology and Pharmaceutics (all)
CiteScore
5.00
自引率
0.00%
发文量
1646
审稿时长
1 weeks
期刊介绍: F1000Research publishes articles and other research outputs reporting basic scientific, scholarly, translational and clinical research across the physical and life sciences, engineering, medicine, social sciences and humanities. F1000Research is a scholarly publication platform set up for the scientific, scholarly and medical research community; each article has at least one author who is a qualified researcher, scholar or clinician actively working in their speciality and who has made a key contribution to the article. Articles must be original (not duplications). All research is suitable irrespective of the perceived level of interest or novelty; we welcome confirmatory and negative results, as well as null studies. F1000Research publishes different type of research, including clinical trials, systematic reviews, software tools, method articles, and many others. Reviews and Opinion articles providing a balanced and comprehensive overview of the latest discoveries in a particular field, or presenting a personal perspective on recent developments, are also welcome. See the full list of article types we accept for more information.
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