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β-葡聚糖诱导的免疫启动可预防斜带石斑鱼神经坏死病毒感染。

Beta glucan induced immune priming protects against nervous necrosis virus infection in sevenband grouper.

机构信息

Department of Aqualife Medicine, Chonnam National University, Yeosu, 59629, Republic of Korea.

Department of Aqualife Medicine, Chonnam National University, Yeosu, 59629, Republic of Korea.

出版信息

Fish Shellfish Immunol. 2022 Feb;121:163-171. doi: 10.1016/j.fsi.2022.01.005. Epub 2022 Jan 10.

DOI:10.1016/j.fsi.2022.01.005
PMID:35017048
Abstract

In the present study, we studied the effect of β-glucan on the activation of antiviral immune responses against nervous necrosis virus (NNV) taking into consideration the role of innate immune training. Sevenband grouper primary macrophages showed an attenuated proinflammatory response and elevated antiviral response to NNV infection. In vitro, priming of β-glucan enhanced macrophage viability against NNV infection which is associated with the activation of sustained inflammatory cytokines gene expression. Observations were clear to understand that NLR Family CARD Domain Containing 3 (NLRC3) and caspase-1 activation and subsequent IL-1β production were reduced in β-glucan-primed macrophages. Subsequent markers for training including Lactate and abundance of HIF-1α were elevated in the cells following training. However, the lactate dehydrogenase (LDH) concentrations remained stable among the β-glucan stimulated infected and uninfected groups suggesting similar macrophage health in both groups. In vivo, the NNV-infected fish primed with β-glucan had a higher survival rate (60%) than the control NNV-infected group (40%). Our findings demonstrate that β-glucan induced protective responses against NNV infection and studies are underway to harness its potential applicability for prime and boost vaccination strategies.

摘要

在本研究中,我们研究了β-葡聚糖对神经坏死病毒(NNV)抗病毒免疫反应激活的影响,同时考虑了先天免疫训练的作用。七带石斑鱼原代巨噬细胞表现出炎症反应减弱和对 NNV 感染的抗病毒反应增强。在体外,β-葡聚糖的预刺激增强了巨噬细胞对 NNV 感染的存活能力,这与持续炎症细胞因子基因表达的激活有关。观察结果清楚地表明,β-葡聚糖预刺激的巨噬细胞中 NLR 家族 CARD 结构域包含 3(NLRC3)和半胱天冬酶-1 的激活以及随后的 IL-1β产生减少。随后的训练标记物,包括乳酸和 HIF-1α的丰度,在训练后细胞中升高。然而,β-葡聚糖刺激的感染和未感染组之间的乳酸脱氢酶(LDH)浓度保持稳定,表明两组巨噬细胞的健康状况相似。在体内,用β-葡聚糖预刺激的 NNV 感染鱼的存活率(60%)高于对照 NNV 感染组(40%)。我们的研究结果表明,β-葡聚糖诱导了对 NNV 感染的保护性反应,目前正在研究利用其作为初级和增强疫苗接种策略的潜在适用性。

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