Journal
INFLAMMATION RESEARCH
Volume 66, Issue 8, Pages 691-700Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00011-017-1050-6
Keywords
MUC18/Muc18; Inflammation; Mucin; Airway epithelium
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Funding
- National Institutes of Health [R01 HL122321, R01 AI106287]
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To evaluate the effects of MUC18 on IL-13-mediated airway inflammatory responses in human airway epithelial cells and in mice. Primary normal human tracheobronchial epithelial (HTBE) cells, wild-type (WT) and Muc18 knockout (KO) mice, and mouse tracheal epithelial cells (mTECs) were utilized. 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. 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. 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). These results implicate MUC18 as a potential enhancer of airway inflammation in a type 2 cytokine (e.g., IL-13) milieu.
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