Fig. 5

Proposed novel caspase-1 working models. a Experimentally identified substrates and interaction proteins indicate that caspase-1 may traffic to subcellular locations other than the cytosol. Caspase-1 gets activated in situ in the nucleus by novel nuclear inflammasomes and caspase-1 cleaves its substrates in exocytotic secretory pathways including exosomes to propagate inflammation to neighboring and remote cells. A-CASP1: activated caspase-1. ① The release of extracellular vesicles (Evs) as a mode of intercellular communication. ② Caspase-1 by inflammasome complexes is directly linked to exosomes and microvesicles (EMVs) that acts as a transport vehicle in this pathway. ③ Exosomes and microvesicles (EMVs) can transmit signals and molecules to neighboring cells via a non-viral pathway of intercellular vesicle traffic. ④ Breast cancer cells induce pro-inflammatory activity of distant macrophages through circulating exosomal vesicles secreted during cancer progression—so-called cancer propagation. b Novel model of extracellular trafficking of caspase-1 and inflammasome components propagate inflammation to neighboring and remote cells