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. Author manuscript; available in PMC: 2009 Mar 13.
Published in final edited form as: J Immunol. 2008 Dec 15;181(12):8504–8512. doi: 10.4049/jimmunol.181.12.8504

FIGURE 7.

FIGURE 7

IL-17A and 1,25D3 increase cathelicidin by activation of MEK-ERK. To investigate the role of MEK-ERK signaling in IL-17A-induced cathelicidin, NHEK were treated with the specific MEK inhibitor PD98059 (20 μM) before stimulation with IL-17A or 1,25D3. Inhibition of MEK-ERK blocked increased cathelicidin by IL-17A in the presence of 1,25D3. A, The 1,25D3-induced cathelicidin was also diminished. To investigate whether MEK-ERK was involved in induction of other innate immune genes by IL-17A, NHEK were treated with PD98059 and subsequently stimulated with 1,25D3 (10−8 M), IL-17A (10 ng/ml), or the combination. B, Again, inhibition of MEK-ERK blocked induction of HBD2. Data are mean ± SD of a single experiment performed in triplicate and are representative of three independent experiments.*, p < 0.05 and **, p < 0.01, determined by Student’s t test. C, The inhibitory effect of PD98059 on MEK-ERK was confirmed by Western blot analyses of phospho-p44/p42. Similar to cathelicidin mRNA expression, inhibition of MEK-ERK signaling blocked IL-17A with 1,25D3-enhanced cathelicidin peptide hCAP18.