Pneumologie 2015; 69 - A12
DOI: 10.1055/s-0035-1548642

The effect of IL-17A deficiency on infection and inflammation is strain dependent in acute murine pneumonia

B Wonnenberg 1, M Voss 1, A Honecker 1, M Bischoff 3, C Meier 2, T Tschernig 2, R Bals 1, C Beisswenger 1
  • 1Department of Internal Medicine V – Pulmonology, Allergology and Respiratory Critical Care Medicine, Saarland University, Homburg
  • 2Institute of Anatomy and Cell Biology, Saarland University, Homburg
  • 3Institute of Medical Microbiology and Hygiene, Saarland University, Homburg

Background: Bacterial pneumonia is worldwide a leading cause of mortality. Acute and chronic inflammations leading to destruction of lung tissue, impaired pulmonary gas exchange, and lung edema are characteristic hallmarks of severe pneumonia. IL-17A has a function in the host defense against a variety of bacterial and fungal pathogens. It was the aim of this study to examine the role of IL-17A during acute murine pneumonia.

Methods: C57BL/6 mice and C57BL/6 mice deficient for IL-17A were intranasally infected with Pseudomonas aeruginosa and Streptococcus pneumoniae for 48 hours. Survival rates and bacterial clearance from the lungs were determined. Alveolar cells were determined in bronchoalveolar lavage fluids. Measurements of cytokines in the lungs and plasma were performed.

Results: Bacterial clearance and survival were significantly increased in mice deficient for IL-17A infected with P. aeruginosa compared to corresponding WT mice. Numbers of total immune cells and concentrations of the inflammatory mediator KC were reduced in lungs of IL-17A deficient mice infected P. aeruginosa. Concentrations of KC were reduced in plasma of of IL-17A deficient mice infected P. aeruginosa. Bacterial clearance from the lungs was decreased in IL-17A deficient mice infected with S. pneumoniae.

Conclusions: These data show that the impact of IL-17A deficiency on bacterial clearance and pulmonary inflammation depends on the infecting bacterial strain in acute murine pneumonia.