Confirmation of processed IL-1ß is an indirect way to assess active caspase-1 activation. Activation of caspase-1 of course is the halmark of inflammasome formation. Immunostaining may detect pro-IL-1ß which is upregulated by NF-kB signaling and not necessarily involving inflammasome activation. I suppose anti-IL-1ß IP could be done followed by LC-MS/MS if you would want to go overboard. Go with immunoblot/western. :-)

For sure the best way to assess inflammasome activation (which can occur independently of signal 1 (i.e an NF-kB inducing signal that upregulates expression of proIL-1 and NLRP3)) is to do a western blot on the supernatant of your cells with an anti-caspase 1 antibody able to detect the p20 subunit (rabbit anti human-cleaved caspase1 clone D57A2 from Cell Signaling). Indeed, after activation and cleavage, the p20 subunit is secreted in the supernatant and easily detectable.

Hope that helps.

@ Björn & Francesco. That rabbit clone from Cell Signaling is a good one. I agree.

Thanks so far for all the constructive suggestions. But, what about detection in vivo, e.g. in inflammatory animals models? Is there a possibility monitor inflammasomes with immunohistochemistry?

Depending on wich in vivo model you do, it's quite easy. If you do the IL-1 dependent MSU-induced peritonitis model, you can harvest inflammatory cells recruited to the peritoneum and do as before immunoblot analysis for caspase 1 activation. I have one publication where whe describe all this. check on my profile, the paper about Type I interferon

cheers