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. Author manuscript; available in PMC: 2018 Oct 15.
Published in final edited form as: J Immunol. 2017 Sep 15;199(8):2885–2895. doi: 10.4049/jimmunol.1700870

Figure 2. Viral infection augments LPS-induced FM IL-1β processing and secretion through activation of the NLRP3 inflammasome.

Figure 2

(A) Human FM explants were treated with (A) No treatment (NT), LPS (100ng/ml), MHV-68 (1.5×104/ml PFU) or both MHV-68 and LPS (n=7). Lysates were evaluated by Western blot for expression of pro-IL-1β (31kDa) and the 17kDa active form. Blots are from one representative experiment. Bar charts show pro- and active-IL-1β expression as determined by densitometry and normalized to β-actin (n=4–5). (B & C) Human FM explants were treated with NT, LPS, MHV-68 or both MHV-68 and LPS in the presence of either media or (B) a caspase-1 inhibitor (1µM) (n=6); or (C) the NLRP3 inhibitor, MNS (10µM) (n=5). Supernatants were measured for IL-1β by ELISA. *p<0.05 relative to the NT control unless otherwise indicated. Data are expressed as mean±SEM.