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. Author manuscript; available in PMC: 2017 Apr 1.
Published in final edited form as: Eur J Immunol. 2016 Jan 20;46(4):897–911. doi: 10.1002/eji.201546015

Figure 9. IL-1β release in response to L. major infection is dependent on caspase-1 and Nlrp3 inflammasome activation in vitro.

Figure 9

(A) Immunoblotting for IL-1β in culture supernatants (SN) from BMDMs prepared from wt or caspase-1/11−/− mice treated or not with LPS (50 ng/ml) and infected or not with LmSd or LmFn metacyclic promastigotes at an MOI of 1:8 for 6 hr. The cell lysates (XT) were blotted with antibodies against pro-IL-1β, pro-caspase–1, and β–actin. (B) Immunoblotting for mature IL-1β in culture supernatants from BMDMs prepared from wt or Nlrp3−/− mice treated or not with LPS (50 ng/ml) and infected with LmSd metacyclic promastigotes at an MOI of 1:8 for 0.5–6 hr. (C) IL-1β concentration in culture supernatants of BMDMs from wt or caspase-1/11−/− mice pre-treated or not with LPS (50 ng/ml) for 5 hrs, followed by infection with LmSd metacyclic promastigotes at different MOIs for 6 hr. Values shown are means ± SD of quadruplicate assays. (D) Conditions of infection and activation of BMDMs are identical to (C), but cells were also pre-treated or not for 5 hr with the selective caspase-1 inhibitor Z-WEHD-FMK or control Z-FA-FMK. ** p<0.01; *** p<0.001.