• Eva Pastille, Stephanie Pohlmann, Florian Wirsdörfer, Anna Reib, and Stefanie B Flohé.
• Surgical Research, Department of Trauma Surgery, University Hospital Essen, University Duisburg-Essen, Essen, Germany Institute for Medical Microbiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
• Innate Immun. 2015 Feb 1; 21 (2): 115-26.

AbstractImpaired resistance to Pseudomonas aeruginosa-induced pneumonia after cecal ligation and puncture (CLP), a mouse model for human polymicrobial sepsis, is associated with decreased IFN-γ, but increased IL-10, levels in the lung. We investigated the so far unknown mechanisms underlying this reduced IFN-γ synthesis in CLP mice. CD11b(+) NK cells, but not T or NKT cells in the lung were impaired in IFN-γ synthesis upon challenge with Pseudomonas in vitro and in vivo after CLP. The inhibition of NK cells was independent of IL-10. IFN-γ synthesis of NK cells was only partly restored by addition of recombinant IL-12. Accessory cells including dendritic cells and alveolar macrophages were required for maximal IFN-γ secretion. But accessory cells of CLP mice suppressed the IFN-γ secretion from naive lung leukocytes. In turn, naive accessory cells were unable to restore the IFN-γ production from lung leukocytes of CLP mice. Thus, a disturbed interaction of accessory cells and NK cells is involved in the impaired IFN-γ release in response to Pseudomonas in the lung of CLP mice. Considering the importance of IFN-γ in the immune defense against bacteria the dysfunction of accessory cells and NK cells might contribute to the enhanced susceptibility to Pseudomonas after CLP.© The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.

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