Institute of Medicine, Chung Shan Medical University, No. 110, Sec. 1, Chien-Kuo N. Road, Taichung, Taiwan 402; Department of Emergency Medicine, Changhua Christian Hospital, Changhua, Taiwan.
Department of Emergency Medicine, Changhua Christian Hospital, Changhua, Taiwan.
J Microbiol Immunol Infect. 2019 Dec;52(6):911-919. doi: 10.1016/j.jmii.2019.03.002. Epub 2019 Mar 23.
Asthma is a heterogeneous inflammatory disorder of the airway. A Th2 response usually contributes to high levels of allergen-specific IgE and eosinophilic airway inflammation. Several findings have demonstrated that neutrophils, not eosinophils, are the major inflammatory cells in chronic asthma patients with steroid-resistance. Lactobacillus rhammosus GG (LGG) exhibits anti-inflammatory properties on OVA-induced acute airway inflammation.
We hypothesized that orally administrated LGG should reduce airway remodeling in chronic experimental models.
Female Balb/c mice were sensitized with OVA. LGG was used to investigate whether oral administrations of LGG inhibited OVA-induced airway inflammation in a chronic asthma model and the different intervention times between LGG pre-treatment and post-treatment groups. BALF was analyzed with Liu's stain and ELISA assay. Lung histopathology was assayed with HE, IHC and Masson's trichrome staining. Lung tissues were assayed with PCR (T-bet, GATA3, RORrt and Foxp3). Many cytokines were detected in the serum and BALF.
LGG significantly decreased the number of infiltrating inflammatory cells. We also found that the oral LGG group suppressed not only Th2 cytokine, but also IL-17, TNF-α and HMGB1 in the BALF levels. However, GATA3 and RORrt decreased significantly in the RNA level in the LGG groups, but the T-bet and Foxp3 increased in the RNA level.
LGG not only had anti-inflammatory effects on OVA-induced airway inflammation, but also improved airway remodeling and collagen expression in the chronic asthma mouse model. Moreover, LGG might be an additional or supplementary therapy for allergic airway diseases.
哮喘是一种气道的异质性炎症性疾病。Th2 反应通常导致过敏原特异性 IgE 和嗜酸性粒细胞性气道炎症水平升高。多项研究结果表明，在类固醇耐药的慢性哮喘患者中，中性粒细胞而非嗜酸性粒细胞是主要的炎症细胞。鼠李糖乳杆菌 GG（LGG）对 OVA 诱导的急性气道炎症具有抗炎作用。
我们假设口服 LGG 应减少慢性实验模型中的气道重塑。
雌性 Balb/c 小鼠用 OVA 致敏。使用 LGG 来研究口服 LGG 是否能抑制慢性哮喘模型中 OVA 诱导的气道炎症，以及 LGG 预处理组和后处理组之间不同的干预时间。用 Liu 染色和 ELISA 检测 BALF。用 HE、IHC 和 Masson 三色染色检测肺组织病理学。用 PCR（T-bet、GATA3、RORrt 和 Foxp3）检测肺组织。检测血清和 BALF 中的多种细胞因子。
LGG 显著减少了浸润性炎症细胞的数量。我们还发现，口服 LGG 组不仅抑制了 BALF 水平中的 Th2 细胞因子，还抑制了 IL-17、TNF-α 和 HMGB1。然而，LGG 组的 GATA3 和 RORrt 在 RNA 水平上显著下降，但 T-bet 和 Foxp3 在 RNA 水平上增加。
LGG 不仅对 OVA 诱导的气道炎症具有抗炎作用，而且改善了慢性哮喘小鼠模型中的气道重塑和胶原表达。此外，LGG 可能是过敏性气道疾病的一种额外或补充治疗方法。
