Skip to main content
. Author manuscript; available in PMC: 2020 Sep 11.
Published in final edited form as: Eur J Immunol. 2019 Apr 3;49(7):1023–1037. doi: 10.1002/eji.201848016

Figure 7.

Figure 7.

Mechanisms of activation of NLRP3 inflammasome and its regulation by nitric oxide in BMDMs infected with B. abortus. B. abortus infection induces lysosomal acidification, cathepsin B release and potassium (K+) efflux and leads to Caspase-1 activation and IL-1β secretion. These events can be inhibited by chloroquine, Ca074Me and Glibenclamide/KCl, respectively, without significant changes in pro-caspase-1 and pro-IL-1β expression. The NLRP3-dependent IL-1β production is also impaired by NO, produced either by macrophage iNOS or as an intermediate metabolite of the bacterial denitrification process. Chl: chloroquine; Glib: glibenclamide; ROS: reactive oxygen species.