Platelets facilitate primary progressive tuberculosis by restricting the oxidative burst in phagocytes

Tuberculosis (TB) remains the leading cause of death by a single infectious agent worldwide. Despite decades of active research, host factors which underly susceptibility to Mycobacterium tuberculosis (Mtb), the etiologic agent of TB, are still ill defined. We investigated the role of platelets (PLTs) during primary TB in mice as these cells were recently assigned multiple immunological functions. PLTs were present at the site of infection, formed aggregates with different myeloid subsets during experimental TB and such aggregates were detected also in TB patients. PLTs were detrimental during the early phase of infection and this effect was uncoupled from their canonical activation. PLTs left lung cell dynamics and patterns of anti-mycobacterial T-cell responses unchanged. PLTs hampered cell autonomous defense by restricting production of reactive oxygen species (ROS) in lung residing myeloid cells. Thus, PLTs orchestrate immunity in TB by modulating innate immune responsiveness during primary lung infection and may be amenable to new interventions for this deadly disease. Design include 8 control samples and 8 samples collected 36h after PLT depletion antibody or isotype control injection on d14 p.i. In total 16 samples collected from M. musculus (strain: 129S2) BALs. There was no replicats.