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Vitamin A supplement after neonatal Streptococcus pneumoniae pneumonia inhibits the progression of experimental asthma by altering CD4+T cell subsets.
Scientific Reports ( IF 3.8 ) Pub Date : 2020-03-06 , DOI: 10.1038/s41598-020-60665-4
Yonglu Tian 1, 2 , Qinqin Tian 1, 2 , Yi Wu 1, 2 , Xin Peng 1, 2 , Yunxiu Chen 1, 2 , Qinyuan Li 1, 2 , Guangli Zhang 3 , Xiaoyin Tian 1, 2 , Luo Ren 2 , Zhengxiu Luo 3
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Studies demonstrated that pneumonia can decrease vitamin A productions and vitamin A reduction/deficiency may promote asthma development. Our previous study showed that neonatal Streptococcus pneumoniae (S. pneumoniae) infection promoted asthma development. Whether neonatal S. pneumoniae pneumonia induced asthma was associated with vitamin A levels remains unclear. The aim of this study was to investigate the effects of neonatal S. pneumoniae pneumonia on vitamin A expressions, to explore the effects of vitamin A supplement after neonatal S. pneumoniae pneumonia on adulthood asthma development. Non-lethal S. pneumoniae pneumonia was established by intranasal inoculation of neonatal (1-week-old) female BALB/c mice with D39. S. pneumoniae pneumonia mice were supplemented with or without all-trans retinoic acid 24 hours after infection. Vitamin A concentrations in lung, serum and liver were measured post pneumonia until early adulthood. Four weeks after pneumonia, mice were sensitized and challenged with OVA to induce allergic airway disease (AAD). Twenty-four hours after the final challenge, the lungs and bronchoalveolar lavage fluid (BALF) were collected to assess AAD. We stated that serum vitamin A levels in neonatal S. pneumoniae pneumonia mice were lower than 0.7µmol/L from day 2-7 post infection, while pulmonary vitamin A productions were significantly lower than those in the control mice from day 7-28 post infection. Vitamin A supplement after neonatal S. pneumoniae pneumonia significantly promoted Foxp3+Treg and Th1 productions, decreased Th2 and Th17 cells expressions, alleviated airway hyperresponsiveness (AHR) and inflammatory cells infiltration during AAD. Our data suggest that neonatal S. pneumoniae pneumonia induce serum vitamin A deficiency and long-time lung vitamin A reduction, vitamin A supplement after neonatal S. pneumoniae pneumonia inhibit the progression of asthma by altering CD4+T cell subsets.

中文翻译:

新生儿肺炎链球菌肺炎后补充维生素A可通过改变CD4 + T细胞亚群来抑制实验性哮喘的发展。

研究表明,肺炎可以减少维生素A的产生,而维生素A的减少/缺乏则可以促进哮喘的发展。我们先前的研究表明,新生儿肺炎链球菌(S. pneumoniae)感染可促进哮喘的发展。新生儿肺炎链球菌引起的肺炎是否与维生素A水平相关尚不清楚。这项研究的目的是调查新生儿肺炎链球菌肺炎对维生素A表达的影响,探讨新生儿肺炎链球菌肺炎后补充维生素A对成年哮喘发展的影响。非致命性肺炎链球菌肺炎是通过鼻内接种D39新生(1周龄)雌性BALB / c小鼠而建立的。感染后24小时,补充或不补充全反式视黄酸补充肺炎链球菌肺炎小鼠。肺炎后直至成年早期测量肺,血清和肝脏中的维生素A浓度。肺炎后四周,将小鼠致敏并用OVA攻击以诱发过敏性气道疾病(AAD)。最后一次攻击后二十四小时,收集肺和支气管肺泡灌洗液(BALF)以评估AAD。我们指出,从感染后第2-7天开始,新生儿肺炎链球菌肺炎小鼠的血清维生素A水平低于0.7µmol / L,而从感染后第7-28天开始,肺部维生素A的产生显着低于对照组小鼠。新生儿肺炎链球菌肺炎后补充维生素A可以显着促进Foxp3 + Treg和Th1的产生,降低Th2和Th17细胞的表达,减轻AAD期间的气道高反应性(AHR)和炎性细胞浸润。
更新日期:2020-03-06
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