Chia-Ta Wu1, Fei-Hung Lin2, Yu-Tzu Lee3, Min-Sho Ku4, Ko-Haung Lue5. 1. 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. Electronic address: allenpig1102@gmail.com. 2. Department of Emergency Medicine, Changhua Christian Hospital, Changhua, Taiwan. 3. Institute of Medicine, Chung Shan Medical University, No. 110, Sec. 1, Chien-Kuo N. Road, Taichung, Taiwan 402. 4. School of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Pediatrics, Chung Shan Medical University Hospital, Taichung, Taiwan. Electronic address: cshy539@csh.org.tw. 5. Institute of Medicine, Chung Shan Medical University, No. 110, Sec. 1, Chien-Kuo N. Road, Taichung, Taiwan 402; School of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Pediatrics, Chung Shan Medical University Hospital, Taichung, Taiwan; College of Biological Science and Technology, National Chiao Tung University, Hsinchu, Taiwan. Electronic address: cshy095@csh.org.tw.
Abstract
BACKGROUND: 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. OBJECTIVE: We hypothesized that orally administrated LGG should reduce airway remodeling in chronic experimental models. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: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 asthmapatients with steroid-resistance. Lactobacillus rhammosus GG (LGG) exhibits anti-inflammatory properties on OVA-induced acute airway inflammation. OBJECTIVE: We hypothesized that orally administrated LGG should reduce airway remodeling in chronic experimental models. METHODS: 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. RESULTS: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. CONCLUSIONS:LGG not only had anti-inflammatory effects on OVA-induced airway inflammation, but also improved airway remodeling and collagen expression in the chronic asthmamouse model. Moreover, LGG might be an additional or supplementary therapy for allergic airway diseases.