IMMUNOLOGY2026™ Conference Recordings For Attendees-A Novel Mediator Extracellular Caspase-1 Worsens Acute Lung Injury in Sepsis

A Novel Mediator Extracellular Caspase-1 Worsens Acute Lung Injury in Sepsis

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Video Summary

Researchers found that extracellular caspase-1 is released during sepsis through gasdermin D pores and acts as an inflammatory mediator. In patient plasma, septic mice, and macrophage experiments, extracellular caspase-1 increased inflammatory cytokines and organ injury, especially in the lungs. It worked by binding to TLR4, a key receptor for inflammation. The team designed a peptide inhibitor, C16, which blocked caspase-1–TLR4 interaction. In septic mice, C16 reduced inflammation, lung edema, lung injury, and improved 10-day survival. The study suggests C16 may be a potential therapy for sepsis-induced acute lung injury.

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Date April 16, 2026 3:45 PM - 3:57 PM

Room 156

Session Pathogen Sensing and Innate Immune Responses

Speaker Kohei Ishikawa

Track Innate Immune Responses and Host Defense: Molecular Mechanisms (INM)

Year 2026

Keywords

extracellular caspase-1

sepsis

TLR4 signaling

C16 peptide inhibitor

acute lung injury

April 16, 2026 3:45 PM - 3:57 PM

156

Pathogen Sensing and Innate Immune Responses

Kohei Ishikawa

Innate Immune Responses and Host Defense: Molecular Mechanisms (INM)

2026