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Published on: July 7, 2017
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MUC18 regulates IL-13-mediated airway inflammatory response
Connor Stevenson1, Di Jiang1, Niccolette Schaefer1
1Department of Medicine, National Jewish Health, 1400 Jackson Street, Room A639, Denver, CO, 80206, USA.
Summary
MUC18 may enhance airway inflammation driven by IL-13. Reducing MUC18 decreased inflammatory markers, while increasing it worsened responses in airway cells and mice.
Area of Science:
- Immunology
- Respiratory Medicine
- Molecular Biology
Background:
- Interleukin-13 (IL-13) is a key mediator of type 2 airway inflammation.
- The role of MUC18 in IL-13-induced inflammatory responses requires further elucidation.
Purpose of the Study:
- To investigate the effect of MUC18 on IL-13-mediated airway inflammation.
- To assess MUC18's role in human airway epithelial cells and mouse models.
Main Methods:
- Utilized primary human tracheobronchial epithelial (HTBE) cells, wild-type (WT) and Muc18 knockout (KO) mice.
- Assessed MUC18's impact via siRNA and lentiviral overexpression in HTBE cells.
- Quantified inflammatory markers using PCR, Western Blot, ELISA, and BAL cell analysis.
Main Results:
- MUC18 siRNA reduced IL-13-induced eotaxin-3 in HTBE cells.
- MUC18 overexpression enhanced IL-13-induced eotaxin-3 in HTBE cells.
- IL-13-treated Muc18 KO mice showed a trend towards lower neutrophil percentages in BAL fluid compared to WT mice.
Conclusions:
- MUC18 appears to enhance airway inflammation in the context of type 2 cytokines like IL-13.
- MUC18 is implicated as a potential therapeutic target for IL-13-driven airway diseases.
