Orally Administered Salacia reticulata Extract Reduces H1N1 Influenza Clinical Symptoms in Murine Lung Tissues Putatively Due to Enhanced Natural Killer Cell Activity.

Orally Administered Salacia reticulata Extract Reduces H1N1 Influenza Clinical Symptoms in Murine Lung Tissues Putatively Due to Enhanced Natural Killer Cell Activity.
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DOI:
10.3389/fimmu.2016.00115
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发表时间:
2016
影响因子:
7.3
通讯作者:
Inoue R
Inoue R
中科院分区:
医学2区
文献类型:
--
作者:
Romero-Pérez GA;Egashira M;Harada Y;Tsuruta T;Oda Y;Ueda F;Tsukahara T;Tsukamoto Y;Inoue R

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流感是呼吸道感染的主要原因。尽管大多数病例不需要进一步住院治疗,但流感会定期在人类中引起流行病,可能会感染并杀死数百万人。为了应对这一威胁,需要每年开发新疫苗,以匹配新出现的流感病毒株,并增强对现有疫苗的抵抗力。因此,需要寻找和开发新的抗流感病毒剂作为当前治疗的替代品。在这里,我们测试了五层龙 (SSRE) 茎和根提取物对感染 H1N1 流感病毒的小鼠的抗病毒作用,SSRE 是一种富含植物化学物质(如五层龙醇、可他醇和儿茶素)的植物。口服0.6mg/天的SSRE后,80%的小鼠咳嗽发生率下降,并且仅检测到1例严重肺部炎症。此外,与给予干酪乳杆菌 JCM1134(一种先前显示有助于增加体外自然杀伤 (NK) 细胞活性的菌株)的小鼠相比,给予 SSRE 的小鼠在脾细胞和肺细胞中分别表现出更高且相等的 NK 细胞活性,且效应细胞与靶细胞比率较高。接下来,为了测试 SSRE 在没有肠道微生物群的情况下是否能发挥针对流感的保护作用,在接种流感病毒之前给小鼠注射抗生素,然后注射 SSRE。 SSRE 给药诱导脾细胞和肺细胞中 NK 细胞活性的增加,其水平与未接受抗生素治疗的小鼠中检测到的水平相似。根据我们的结果,可以得出结论,SSRE 中的植物化学物质可能通过调节免疫反应(包括增强 NK 细胞活性)发挥针对流感感染的保护作用,尽管某些保护作用不一定是通过调节肠道微生物群来实现的。有必要进一步研究以阐明 SSRE 对流感感染保护作用的分子机制。
Influenza is a major cause of respiratory tract infection. Although most cases do not require further hospitalization, influenza periodically causes epidemics in humans that can potentially infect and kill millions of people. To countermeasure this threat, new vaccines need to be developed annually to match emerging influenza viral strains with increased resistance to existing vaccines. Thus, there is a need for finding and developing new anti-influenza viral agents as alternatives to current treatments. Here, we tested the antiviral effects of an extract from the stems and roots of Salacia reticulata (SSRE), a plant rich in phytochemicals, such as salacinol, kotalanol, and catechins, on H1N1 influenza virus-infected mice. Following oral administration of 0.6 mg/day of SSRE, the incidence of coughing decreased in 80% of mice, and only one case of severe pulmonary inflammation was detected. Moreover, when compared with mice given Lactobacillus casei JCM1134, a strain previously shown to help increase in vitro natural killer (NK) cell activity, SSRE-administered mice showed greater and equal NK cell activity in splenocytes and pulmonary cells, respectively, at high effector cell:target cell ratios. Next, to test whether or not SSRE would exert protective effects against influenza in the absence of gut microbiota, mice were given antibiotics before being inoculated influenza virus and subsequently administered SSRE. SSRE administration induced an increase in NK cell activity in splenocytes and pulmonary cells at levels similar to those detected in mice not treated with antibiotics. Based on our results, it can be concluded that phytochemicals in the SSRE exerted protective effects against influenza infection putatively via modulation of the immune response, including enhancement of NK cell activity, although some protective effects were not necessarily through modulation of gut microbiota. Further investigation is necessary to elucidate the molecular mechanisms underlying the protective effects of SSRE against influenza infection.