Qian L, Lu L, Huang L, Wen Q, Xie J, Jin W, Li H, Jiang L
Department of Pediatrics, Zhongda Hospital, Southeast University, Nanjing, Jiangsu 210009, China; Teaching and Research Section of Pediatrics, Medical College, Southeast University, Nanjing, Jiangsu 210009, China.
Department of Neonatology, Suzhou Municipal Hospital, Suzhou, Jiangsu 210002, China.
Allergol Immunopathol (Madr). 2019 Jan-Feb;47(1):2-11. doi: 10.1016/j.aller.2018.05.004. Epub 2018 Nov 17.
To investigate neonatal maternal separation (NMS) effects on airway inflammation of asthma and potential mechanism using a mouse model.
80 Balb/c neonatal male mice were randomly assigned to NMS and non-NMS groups. Feces were collected on PND21, 28, 35 and 42 to analyze microbiota and short-chain fatty acids (SCFAs). Non-NMS group were then divided into control (group A) and asthma groups (group B), while NMS group was assigned to NMS+asthma (group C) and NMS+SCFAs+asthma groups (group D). Inflammatory cells and eosinophils (EOS) in bronchoalveolar lavage fluid (BALF) were assessed. Pathological changes and cytokines in lung tissue were observed. Protein expression of Occludin and E-cadherin in airway epithelial was examined.
The number of S', diversity index H' and dominance index D', as well as content butyric acid in NMS group C were significantly lower than non-NMS group B (p<0.05). Mice in group C had a higher level of inflammatory cells and EOS compared with group A, B and D. EOS moderate infiltration was found in mice of group B, C and D. Mice in group C had significantly higher levels of cytokines and showed slightly increased bronchial epithelium goblet cells and a small amount of visceral secretions. Occludin and E-cadherin expression in lung in B, C and D groups was depressed, and protein level in group C was significantly lower than group B and D.
NMS is associated with exacerbated inflammation of adult asthma by changing intestinal microflora resulting in butanoic acid decline and airway epithelial barrier damage.
利用小鼠模型研究新生鼠母婴分离（NMS）对哮喘气道炎症的影响及其潜在机制。
将80只Balb/c新生雄性小鼠随机分为NMS组和非NMS组。在出生后第21、28、35和42天收集粪便，分析微生物群和短链脂肪酸（SCFAs）。然后将非NMS组分为对照组（A组）和哮喘组（B组），而NMS组分为NMS+哮喘组（C组）和NMS+SCFAs+哮喘组（D组）。评估支气管肺泡灌洗液（BALF）中的炎症细胞和嗜酸性粒细胞（EOS）。观察肺组织的病理变化和细胞因子。检测气道上皮中紧密连接蛋白（Occludin）和E-钙黏蛋白（E-cadherin）的蛋白表达。
NMS组C的S'数量、多样性指数H'和优势度指数D'以及丁酸含量均显著低于非NMS组B（p<0.05）。与A、B和D组相比，C组小鼠的炎症细胞和EOS水平更高。在B、C和D组小鼠中发现EOS中度浸润。C组小鼠的细胞因子水平显著更高，支气管上皮杯状细胞略有增加，并有少量内脏分泌物。B、C和D组肺组织中Occludin和E-cadherin表达降低，C组蛋白水平显著低于B组和D组。
NMS通过改变肠道微生物群导致丁酸减少和气道上皮屏障损伤，与成年哮喘炎症加剧有关。
