Markus Bosmann

TL;DR: Recent insights into the signaling pathways in immune and phagocytic cells that underlie sepsis and SIRS are discussed and how these might be targeted for therapeutic interventions to reverse or attenuate pathways that lead to lethality during sepsi are considered.

TL;DR: An in vitro human model that simulates the initial apical infection of alveolar epithelium with SARS-CoV-2 is presented, using induced pluripotent stem cell-derived AT2s that have been adapted to air-liquid interface culture and finds a rapid transcriptomic change in infected cells, characterized by a shift to an inflammatory phenotype with upregulation of NF-kB signaling and loss of the matureAlveolar program.

TL;DR: High‐resolution magnetic resonance imaging demonstrated lung damage, edema and consolidation in histone‐injured lungs, confirming the destructive C5a‐dependent effects in lung linked to appearance of extracellular histones.

TL;DR: The present data suggest that IFN-γ may limit biological functions of IL-18 at sites of colonic immune activation by inducing IL- 18BPa production, and down-regulation ofIL-18BPa by sodium butyrate suggests that reinforcement of local IL-17 activity may contribute to actions of this short-chain fatty acid in the colonic microenvironment.

TL;DR: There is accumulating evidence that C5a may suppress inflammatory responses or divert them from Th1 to Th2 responses, impacting the innate immune system, and in experimental polymicrobial sepsis, there is evidence that many of the adverse outcomes can be linked to the roles of C5 a and engagement of its two receptors, C 5aR and C5L2.