Oral administration of heat-killed Lactobacillus kunkeei YB38 improves murine influenza pneumonia by enhancing IgA production.

Oral administration of heat-killed Lactobacillus kunkeei YB38 improves murine influenza pneumonia by enhancing IgA production.
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DOI:
10.12938/bmfh.16-010
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发表时间:
2017
期刊:
Bioscience of microbiota, food and health
影响因子:
--
通讯作者:
Hashimoto K
Hashimoto K
中科院分区:
其他
文献类型:
--
作者:
Asama T;Uematsu T;Kobayashi N;Tatefuji T;Hashimoto K

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流感是重要的呼吸道感染之一,需要特别注意保持健康和卫生。呼吸道上皮分泌的IgA清除流感病毒(IFV)是一种重要的宿主防御机制。因此,我们从蜜蜂花粉中分离出人类唾液IgA分泌启动子——kunkeei乳酸菌YB38 (YB38),并在小鼠模型上研究热杀YB38对IFV感染的预防作用。雌性BALB/c小鼠连续21天口服YB38,然后鼻腔接种IFV。日剂量为100 mg/kg的yb38治疗组在IFV感染后的存活率高于对照组。感染6 d后,yb38 (100 mg/kg)组大鼠呼吸道上皮IgA分泌量显著升高,同一呼吸部位IL-6分泌量及浸润肺泡细胞数量显著减少。此外,IFV感染后出现的肺组织损伤也有所减轻。这些结果表明,YB38剂量诱导感染部位早期和局部IgA分泌,抑制IFV持续感染,阻止炎症免疫细胞浸润或过量IL-6的产生,对肺组织的损伤较小。
Influenza is one of the important respiratory tract infections that require special attention for maintaining health and hygiene. The removal of influenza virus (IFV) by secretory IgA produced by the respiratory epithelium has been reported to be a critical host defense mechanism. Therefore, we isolated Lactobacillus kunkeei YB38 (YB38), the promoter of the salivary IgA secretion in humans, from honeybee pollen and studied the effect of heat-killed YB38 treatment for preventing IFV infection in a mouse model. Female BALB/c mice received YB38 orally for 21 consecutive days and were then inoculated nasally with IFV. The YB38-treated group with a daily dose of 100 mg/kg showed an increased survival rate after IFV infection relative to the control. IgA secretion in the respiratory epithelium in the YB38-treated group (100 mg/kg) was significantly increased after 6 days of infection, while IL-6 production in the same respiratory site and the number of cells infiltrating into alveoli were significantly decreased. Moreover, lung tissue damage that appeared after IFV infection was reduced. These results suggested that the YB38 dose induced early and local IgA secretion at the infection site, inhibited persistent IFV infection, and prevented the infiltration of inflammatory immune cells or production of excessive IL-6, resulting in less damage to lung tissues.