Fungal immunomodulatory protein-fve could modulate airway remodel through by affect IL17 cytokine
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Updated: Feb 26, 2026

Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
Published on: February 18, 2015
Yu-Tzu Lee1, Chia-Ta Wu2, Hai-Lun Sun3
1Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
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.
Insights
FIP-fve effectively reduced airway remodeling and inflammation in a chronic asthma model. This compound suppressed inflammatory cells, Th2 cytokines, and Th17 cells, offering potential as an alternative therapy for allergic airway diseases.
Area of Science:
- Immunology
- Respiratory Medicine
- Pharmacology
Background:
- Asthma is a prevalent allergic disease.
- Previous research indicated FIP-fve reduces inflammation and balances Th1/Th2 in acute models.
- The impact of FIP-fve on airway remodeling in chronic asthma remained unexplored.
Purpose of the Study:
- To investigate the efficacy of orally administered FIP-fve in reducing airway remodeling in chronic allergic asthma models.
- To evaluate FIP-fve's effects on airway inflammation, Th1/Th2 balance, and specific inflammatory markers.
Main Methods:
- A chronic asthma model was established in Balb/c mice using ovalbumin (OVA) challenges.
- Airway inflammation and hyperresponsiveness (AHR) were assessed using a BUXCO system.
- Bronchoalveolar lavage fluid (BALF), serum, and lung tissues were analyzed for inflammatory cells, cytokines, collagen deposition, and matrix metalloproteinase 9 (MMP9) expression.
Main Results:
- FIP-fve significantly reduced inflammatory cell infiltration (neutrophils, eosinophils) and Th2 cytokines while increasing Th1 cytokines in BALF and serum.
- Compared to corticosteroids, FIP-fve demonstrated superior reduction of infiltrating cells.
- Oral FIP-fve suppressed IL-17 and enhanced IL-22, decreased MMP9 expression, collagen deposition, and overall airway remodeling.
Conclusions:
- FIP-fve exhibits significant anti-inflammatory effects in OVA-induced airway inflammation.
- FIP-fve inhibits Th17 cells, leading to reduced airway remodeling and collagen expression.
- FIP-fve presents as a promising alternative therapeutic agent for allergic airway diseases.
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