Blocking Both IL-1β and IL-18 Mitigates the Sepsis Response in Mice

In a murine model, genetic deletion — or simultaneous neutralization — of these two cytokines significantly reduced mortality in experimental forms of sepsis.

Mortality in sepsis is believed to be caused by unbridled inflammation subsequent to cytokine release. Experimentally, the sepsis syndrome can be mimicked by injection of lipopolysaccharide (LPS). In part, LPS induces sepsis by activating the cytokines interleukin (IL)-1β and IL-18. Previous studies exploring this area have been conducted under disparate conditions with different mouse strains and have led to conflicting results. Now, researchers in Europe have used mice with genetic deletion of IL-1β and IL-18 to explore the therapeutic potential of neutralizing these cytokines.

When injected with a lethal dose of LPS, mice deficient in IL-1β and IL-18 had lower mortality and less cellular and organ damage than wild-type mice. When cecal li…

Reviewing Author

Neil M. Ampel, MD

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Editorial BoardsUpToDate

Leadership Positions in Professional SocietiesCoccidioidomycosis Study Group (Past President, Secretary, Treasurer)

Neil M. Ampel, MD

Disclosures

Editorial BoardsUpToDate

Leadership Positions in Professional SocietiesCoccidioidomycosis Study Group (Past President, Secretary, Treasurer)

Blocking Both IL-1β and IL-18 Mitigates the Sepsis Response in Mice

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Reviewing Author