Tenascin-C Deficiency Is Associated With Reduced Bacterial Outgrowth During Klebsiella pneumoniae-Evoked Pneumosepsis in Mice

Mariska T. Meijer, Alex F. de Vos, Brendon P. Scicluna, Joris J. Roelofs, Chérine Abou Fayçal, Gertraud Orend, Fabrice Uhel, Tom van der Poll

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Abstract

Tenascin C (TNC) is an extracellular matrix glycoprotein that recently emerged as an immunomodulator. TNC-deficient (TNC−/−) mice were reported to have a reduced inflammatory response upon systemic administration of lipopolysaccharide, the toxic component of gram-negative bacteria. Here, we investigated the role of TNC during gram-negative pneumonia derived sepsis. TNC+/+ and TNC−/− mice were infected with Klebsiella pneumoniae via the airways and sacrificed 24 and 42 h thereafter for further analysis. Pulmonary TNC protein levels were elevated 42 h after infection in TNC+/+ mice and remained undetectable in TNC−/− mice. TNC−/− mice showed modestly lower bacterial loads in lungs and blood, and a somewhat reduced local—but not systemic—inflammatory response. Moreover, TNC−/− and TNC+/+ mice did not differ with regard to neutrophil recruitment, lung pathology or plasma markers of distal organ injury. These results suggest that while TNC shapes the immune response during lipopolysaccharide-induced inflammation, this role may be superseded during pneumosepsis caused by a common gram-negative pathogen.
Original languageEnglish
Article number600979
JournalFrontiers in immunology
Volume12
DOIs
Publication statusPublished - 11 Mar 2021

Keywords

  • Klebsiella pneumoniae (K. pneumoniae)
  • alarmins
  • immune system
  • innate immunity
  • mice
  • pneumonia
  • sepsis
  • tenascin C

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