How plague bacteria kill immune cells

by @NTNUhealth 21 May 2014
PNAS cover

The article has the cover image for the current issue of PNAS. (May 20, 2014)

Many bacteria kill considerable numbers of host cells upon infection. However, the mechanisms behind the cell death are in many cases unclear. A recent article in PNAS by the the CEMIR-affiliated researcher professor Egil Lien,  describes how the bacteria Yersinia pestis, the causative agent of plague, kills key immune cells called macrophages by apoptosis mediated by kinase RIP1 and caspase-8 together with RIP3.

Apoptosis is often considered to be a “silent” type of cell death. However, we found that the death was accompanied by inflammatory processes via IL-18 and IL-1b generating inflammasomes and transcription factor NF-kB, also via RIP kinases and caspase-8. Importantly, mice deficient in caspase-8 and RIP3 were highly susceptible to bacterial infection, suggesting a key pathway for anti-bacterial defenses.

The article made it to the cover in the current issue of PNAS. Learn more about the image here.

Egil Lien. Foto: NTNU

Professor Egil Lien. Foto: NTNU


Wenga, D. , Marty-Roixa, R., Ganesana, S., Proulxb, M.K., Vladimera, G.I., Kaiserc, W.J., Mocarskic, E.S., Pouliota, K., Chand, F.K., Mellihere, M.A., Harrisf, P.A., Bertinf, J.,  Goughf, P. J., Shayakhmetovg, D.M., Goguenb, J.D., Fitzgeralda, K.A., Silvermana, N., Lien, E. Caspase-8 and RIP kinases regulate bacteria-induced innate immune responses and cell death. PNAS (published online).



You may also like