Pyroptosis, a recently characterised form of programmed cell death prominent in macrophages during bacterial infection, differs from classical apoptosis in that it:

• A Requires cytochrome c release from mitochondria to activate caspase-9
• B Results in cell shrinkage and apoptotic body formation without inflammation
• C Is dependent on RIP kinase-1 and -3 (necroptosis pathway) for execution
• D Is mediated by caspase-1 or caspase-11 activation via inflammasome, causing pro-inflammatory cytokine release and plasma membrane rupture ✓

Explanation

Pyroptosis is an inflammatory form of programmed cell death triggered by inflammasome activation (NLRP3, NLRC4), leading to caspase-1 or caspase-11/4/5 activation. These caspases cleave gasdermin D, whose N-terminal fragment forms pores in the plasma membrane causing cell lysis and release of IL-1β and IL-18. Unlike apoptosis, pyroptosis is inflammatory and does not produce apoptotic bodies. Necroptosis involves RIP kinase-driven MLKL pore formation.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.