Fms-Like Tyrosine Kinase-3 Ligand Attenuates Local and Systemic Infection in a Model of Post-Burn Pneumonia

Shock. 2018 Jun;49(6):721-727. doi: 10.1097/SHK.0000000000000964.

Abstract

Background: Burn injury induces immunosuppression and promotes infection with opportunistic pathogens. Pneumonia and sepsis are leading causes of post-burn morbidity and mortality. Fms-like tyrosine kinase-3 ligand (Flt3L) improves local and systemic resistance to P aeruginosa-associated burn wound infection. This study evaluates the effects of post-burn prophylactic Flt3L treatment on local and systemic infection and inflammation in a murine model of pneumonia and sepsis.

Methods: Mice received a severe scald burn, were treated with Flt3L or vehicle (CTR) for 5 days, and inoculated trans-nasally with P aeruginosa. Lung, blood, and spleen were harvested at 24 and 48 h postinoculation (p.i.) to assess infection (bacterial burden, bacteremia, distant organ manifestation) and inflammation (interleukin-6 (IL-6) and myeloperoxidase (MPO) levels). Histology correlated infection and inflammation parameters with morphology. Survival at various bacterial concentrations was monitored for 14 days p.i.

Results: Bacterial burden was significantly reduced in lung and spleen of Flt3L-treated mice. Flt3L treatment was associated with decreased signs of pulmonary inflammation (reduced wet weight and IL-6 levels), lower incidences of bacteremia and septic distant organ manifestation, and reduced systemic inflammation (IL-6 and MPO). Histologically, reduced alveolar and peribronchiolar neutrophil and lymphocyte infiltration indicated attenuated pulmonary inflammation after Flt3L treatment. Overall survival was comparable between groups for all doses of P aeruginosa, but mortality delayed in the Flt3L-treated group.

Conclusion: Prophylactic treatment with Flt3L could augment antimicrobial therapy of post-burn pneumonia through improvement of the initial host response to challenge with P aeruginosa, attenuate local, and systemic inflammation as well as septic pathogen dissemination.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bacteremia / drug therapy
  • Bacteremia / metabolism*
  • Bacteremia / microbiology
  • Bacteremia / pathology
  • Burns / drug therapy
  • Burns / metabolism*
  • Burns / microbiology
  • Burns / pathology
  • Disease Models, Animal
  • Interleukin-6 / metabolism
  • Male
  • Membrane Proteins / antagonists & inhibitors
  • Membrane Proteins / metabolism*
  • Mice
  • Mice, Inbred BALB C
  • Pneumonia, Bacterial / drug therapy
  • Pneumonia, Bacterial / metabolism*
  • Pneumonia, Bacterial / microbiology
  • Pneumonia, Bacterial / pathology
  • Pseudomonas Infections / drug therapy
  • Pseudomonas Infections / metabolism*
  • Pseudomonas Infections / pathology
  • Pseudomonas aeruginosa*

Substances

  • Interleukin-6
  • Membrane Proteins
  • flt3 ligand protein
  • interleukin-6, mouse