Topic: GP130

Chemotherapy with Temozolomide (TMZ) is a mainstay for the treatment of primary brain tumors (glioblastomas; GBM). However, drug efficacy is reduced through a profound ability of GBM cells for DNA-repair and by the blood tumor barrier (BTB), which restricts intratumoral TMZ accumulation. Coherently, GBM almost invariably relapse with fatal outcome. We here show that GBM associated myeloid cells (GAM) simultaneously induce chemoresistance on the genetic and the vascular level by activating GP130 receptor signaling, which can be addressed therapeutically. After performing transcriptomic screens

Interleukin 6 (IL-6), its receptor (IL-6R), with the IL-6 signal transducer gp130 (IL-6ST) are well known regulators of innate immunity but also affect neuron morphology and function. More recent evidence suggests that they also play a significant role in shaping microbiota composition and gut-barrier function (1). However, the exact pathways and mechanisms are still elusive. We therefore investigated the involvement of functional IL-6 signaling in the bilateral communication between primary afferent neurons and gut microbiota.Transgenic mice with a conditional depletion of gp130 in neurons ex