Immunosuppression after Sepsis: Systemic Inflammation and Sepsis Induce a Loss of Naïve T-Cells but No Enduring Cell-Autonomous Defects in T-Cell Function

• DOI: 10.1371/journal.pone.0115094
• Publication Date: 2014-12-26T18:59:32Z
• Authors: Robby Markwart; Stephanie A. Cond...; Robert P. Requardt; Farina Borken; Katja Schubert; Cynthia Weigel; Michael Bauer; Thomas S. Griffith; Martin Förster; Frank M. Brunkhorst; Vladimir P. Badov...; Ignacio Rubio
• Keywords: Immunosuppression Therapy; Inflammation; 0303 health sciences; Science; T-Lymphocytes; Q; R; Receptors, Antigen, T-Cell; Mice, Transgenic; Adaptive Immunity; 3. Good health; Mice, Inbred C57BL; Disease Models, Animal; Mice; 03 medical and health sciences; Lymphopenia; Sepsis; Medicine; Animals; Cytokines; Humans; Research Article

Sepsis describes the life-threatening systemic inflammatory response (SIRS) of an organism to infection and is leading cause mortality on intensive care units (ICU) worldwide. An acute episode sepsis characterized by extensive release cytokines other mediators resulting in a dysregulated immune organ damage and/or death. This initial pro-inflammatory burst often transits into state suppression characterised loss cells T-cell dysfunction at later disease stages survivors. However, despite these appreciations, precise nature evoked defect immunity post-acute phases SIRS remains unknown. Here we present in-depth functional analysis function SIRS/sepsis. We document that not compromised per cell basis experimental rodent models infection-free (LPS or CpG) septic peritonitis. Transgenic antigen-specific T-cells feature unaltered cytokine if challenged vivo ex with cognate antigens. Isolated CD4+/CD8+ from animals do exhibit defects receptor-mediated activation level receptor-proximal signalling, marker upregulation expansion. SIRS/sepsis induced transient lymphopenia gave rise environment attenuation post stages. Thus, inflammation has impact numbers adaptive immunity, but does major cell-autonomous enduring T-cells.