| First Author | Stevenson C | Year | 2017 |
| Journal | Inflamm Res | Volume | 66 |
| Issue | 8 | Pages | 691-700 |
| PubMed ID | 28451734 | Mgi Jnum | J:309819 |
| Mgi Id | MGI:6709500 | Doi | 10.1007/s00011-017-1050-6 |
| Citation | Stevenson C, et al. (2017) MUC18 regulates IL-13-mediated airway inflammatory response. Inflamm Res 66(8):691-700 |
| abstractText | OBJECTIVE: To evaluate the effects of MUC18 on IL-13-mediated airway inflammatory responses in human airway epithelial cells and in mice. MATERIALS: Primary normal human tracheobronchial epithelial (HTBE) cells, wild-type (WT) and Muc18 knockout (KO) mice, and mouse tracheal epithelial cells (mTECs) were utilized. TREATMENT: Cultured HTBE cells treated with MUC18 siRNA or MUC18 expressing lentivirus were incubated with IL-13 (10 ng/mL) for 24 h. Mice were intranasally instilled with 500 ng of IL-13 for 3 days. mTECs were treated with IL-13 (10 ng/mL) for 3 days. METHODS: PCR was used to measure mRNA expression. Western Blot and ELISAs were used to quantify protein expression. Cytospins of bronchoalveolar lavage (BAL) cells were used to obtain leukocyte differentials. RESULTS: MUC18 siRNA reduced IL-13-mediated eotaxin-3 (183 +/- 44 vs. 380 +/- 59 pg/mL, p < 0.05), while MUC18 overexpression increased IL-13-mediated eotaxin-3 (95 +/- 3 vs. 58 +/- 3 pg/mL, p < 0.05) in HTBE cells. IL-13-treated Muc18 KO mice had a lower percentage of neutrophils in BAL than WT mice (25 +/- 3 vs. 35 +/- 3%, p = 0.0565). CONCLUSIONS: These results implicate MUC18 as a potential enhancer of airway inflammation in a type 2 cytokine (e.g., IL-13) milieu. |
