Yu-Tzu Lee1, Chia-Ta Wu2, Hai-Lun Sun3, Jiunn-Liang Ko4, Ko-Haung Lue5. 1. Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan. Electronic address: tsz312@hotmail.com. 2. Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Emergency Medicine, Changhua Christian Hospital, Changhua, Taiwan. 3. School of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Pediatrics, Chung Shan Medical University Hospital, Taichung, Taiwan. 4. Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan. 5. Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; 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 one of the most common allergic diseases. Our previous studies have reported that FIP-fve in acute allergic mouse model can reduce inflammation, improve the balance of the Th1/Th2 system. However, the effects of reducing airway remodeling on FIP-fve is still unknown. OBJECTIVE: We hypothesized that orally administrated FIP-fve should be able to reduce airway remodeling in chronic allergic models. METHODS: The chronic asthma animal model was established with 6-8 weeks female Balb/c mice. After intranasal challenges with OVA, the airway inflammation and AHR were determined by a BUXCO system. BALF was analyzed with Liu's stain and ELISA assay. Lung histopathologic changes and Collagen deposition were assayed with H&E, Masson's trichrome and IHC stain. RESULTS: FIP-fve significantly decreased the number of infiltrating inflammatory cells and Th2 cytokines and increased Th1 cytokines in BALF and serum compared with the OVA sensitized mice. FIP-fve had a better effect than corticosteroid could reduce infiltrating cells in lung especially neutrophils and eosinophils. We also found that the oral FIP-fve group suppressed IL-17 and enhanced IL-22 in the serum and BALF. In addition, oral FIP-fve decreased MMP9 expression, collagen expression and airway remodeling in lung tissues. CONCLUSION: FIP-fve had anti-inflammatory effects on OVA-induced airway inflammation and an effect to inhibited Th17 cells to reduced airway remodeling and collagen expression. Moreover, FIP-fve might be a potential alternative therapy for allergic airway diseases.
BACKGROUND:Asthma is one of the most common allergic diseases. Our previous studies have reported that FIP-fve in acute allergicmouse model can reduce inflammation, improve the balance of the Th1/Th2 system. However, the effects of reducing airway remodeling on FIP-fve is still unknown. OBJECTIVE: We hypothesized that orally administrated FIP-fve should be able to reduce airway remodeling in chronic allergic models. METHODS: The chronic asthma animal model was established with 6-8 weeks female Balb/c mice. After intranasal challenges with OVA, the airway inflammation and AHR were determined by a BUXCO system. BALF was analyzed with Liu's stain and ELISA assay. Lung histopathologic changes and Collagen deposition were assayed with H&E, Masson's trichrome and IHC stain. RESULTS: FIP-fve significantly decreased the number of infiltrating inflammatory cells and Th2 cytokines and increased Th1 cytokines in BALF and serum compared with the OVA sensitized mice. FIP-fve had a better effect than corticosteroid could reduce infiltrating cells in lung especially neutrophils and eosinophils. We also found that the oral FIP-fve group suppressed IL-17 and enhanced IL-22 in the serum and BALF. In addition, oral FIP-fve decreased MMP9 expression, collagen expression and airway remodeling in lung tissues. CONCLUSION: FIP-fve had anti-inflammatory effects on OVA-induced airway inflammation and an effect to inhibited Th17 cells to reduced airway remodeling and collagen expression. Moreover, FIP-fve might be a potential alternative therapy for allergic airway diseases.