Wednesday, October 18, 2017 - 13:00 to 14:00
CTIR Sir Kenneth and Lady Noreen Murray Seminar Room
Professor Paul Crocker FRSE
Professor Marco Oggioni
University of Leicester
In experimental pneumococcal murine infection, an initial reduction of bacterial load in the blood is followed hours later by a fatal septicaemia. This bottleneck in the invading population is caused by the efficient clearance of pneumococci from the blood by splenic macrophages. However, intracellular bacterial replication occurs within a sub-set of CD169-positive macrophages providing a reservoir for dissemination of bacteria into the blood stream. Intracellular replication of pneumococci within CD169+ splenic macrophages was also observed in an ex vivo porcine model where the microanatomy of the spleen is comparable to humans. Our findings define a paradigm shift for the pneumococcus from an exclusively extracellular pathogen to one with an intracellular phase critical for the pathogenesis of septicaemia. These findings open the door to the development of treatments that target this early, previously unrecognized intracellular phase of bacterial sepsis.