Marion Rother

TL;DR: Genome-wide RNAi screening revealed numerous host factors involved in H. pylori-, but not IL-1β- and TNF-α-dependent NF-κB regulation, highlighting the ALPK1-TIFA axis as a core innate immune pathway.

TL;DR: These findings provide the first evidence for a host cell surface receptor that is exploited for invasion as well as for receptor-mediated intracellular signaling to facilitate chlamydial replication and subverts the host cell and induces apoptosis resistance.

TL;DR: It is demonstrated that inhibition of the p53–MDM2 interaction is sufficient to disrupt intracellular development of Chlamydia and interferes with the pathogen’s anti-apoptotic effect on host cells, highlighting the dependency of the pathogenic on a functional MDM2-p53 axis and lends support to a potentially pro-carcinogenic effect of chlamydial infection.

TL;DR: Elevated levels of methylglyoxal (MG), a small and reactive molecule that is usually a physiological product of various metabolic pathways, and advanced glycation end products (AGE) during mycobacterial infection of macrophages, leading to apoptosis and activation of macocytes are demonstrated, providing first evidence for the involvement of MG and AGE in TB.

TL;DR: By applying a high‐throughput siRNA gain‐of‐function screen interrogating the human kinome, 17 kinases are identified that when targeted by siRNA restored IL‐1β‐dependent NF‐κB translocation in infected cells and it is proposed that agents targeting this signalling pathway might provide selective alternatives for the management of K. pneumoniae pneumonias.