IL-18 contributes to sepsis development during post-natal period

This week PNAS published new study that showed that IL-18 deficiency makes newborn mice resistant to bacterial sepsis. 

Current knowledge about pathophysiology of sepsis is incomplete. In this study, IL-18–null (IL-18−/−) newborn mice showed improved survival when exposed to sepsis-induced bacteria.

Exogenous IL-18 could increase susceptibility of newborn mice to sepsis in absence of adaptive immune system (RAG1−/− mice).

Curiously, TCRδ−/− mice lacking γδT cells [but, unlike RAG1−/− mice, have αβT cells] were resistant to IL-18 effect.

At molecular level, effect of IL-18 on sepsis was dependent of IL-1R signaling 

And also on IL-17 signaling.

In summary, this study expands our knowledge of approaches that can be taken to treat sepsis, for example, Anakinra [an interleukin-1R antagonist] and Cosentyx [anti-interleukin-17A].

David Usharauli