Inflammasomes have been extensively characterized in monocytes and macrophages,
but not in epithelial cells, which are the preferred host cells for many pathogens.
Here we show that gingival and cervical epithelial cells express a functional NLRP3
inflammasome. Infection of gingival cells by Porphyromonas gingivalis leads to
production of pro-IL-1β, but not secretion of the cytokine. Addition of the “danger
signal” ATP to infected gingival cells leads to caspase-1 activation and IL-1β secretion.
In contrast, infection of cervical epithelial cells by Chlamydia trachomatis leads to
activation of caspase-1, through a process requiring the NLRP3 inflammasome. In
monocytes and macrophages, caspase-1 is involved in processing and secretion of pro-
inflammatory cytokines such as IL-1β. However, in cervical epithelial cells, which are
not known to secrete large quantities of IL-1β, caspase-1 has been recently shown to
enhance lipid metabolism. We now show that, in cervical epithelial cells, caspase-1
activation is also required for optimal growth of the intracellular chlamydiae.
Link to video.