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. Author manuscript; available in PMC: 2015 Apr 17.
Published in final edited form as: Nat Commun. 2014 Oct 17;5:5230. doi: 10.1038/ncomms6230

Figure 4. Poly(I:C), but not HSV-1, stimulated IL-1α release is inflammatory caspase dependent.

Figure 4

(a) Human primary keratinocytes were pre-treated with vehicle (white bars) or an inflammatory caspase specific inhibitor (black bars) for 30 min. before addition of medium or 25 μg ml-1 poly(I:C). Culture medium was collected after 12 hours and IL-1α levels determined by ELISA. (b) Mouse primary keratinocytes isolated from wild type (white bars) and inflammatory caspase deficient (black bars) mice were infected with HSV-1 (0.2 MOI) as described in Fig. 1. Control cells were treated with medium only. IL-1α released into the culture medium 24 hours post-infection was quantified using a mouse IL-1α specific ELISA. (a and b) Data points (n = 3) represent means ± s.d. Each experiment was repeated at least twice with similar outcomes. *, P < 0.05 (compared to medium only, t-test); **, P < 0.01.