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Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
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Published on: March 21, 2021

Pulmonary contusion primes systemic innate immunity responses.

J Jason Hoth1, R S Martin, Barbara K Yoza

  • 1Department of General Surgery, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA. jhoth@wfubmc.edu

The Journal of Trauma
|July 11, 2009
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Traumatic lung injury primes the immune system for a worse reaction to infection. Hypertonic saline resuscitation effectively reduced this exaggerated immune response in mice.

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Area of Science:

  • Immunology
  • Trauma Research
  • Critical Care Medicine

Background:

  • Traumatic injury can lead to an amplified immune response to subsequent infections, a phenomenon known as the "second hit."
  • The molecular mechanisms underlying immune priming after traumatic lung injury, specifically pulmonary contusion, are not well understood.
  • This study investigates immune priming following pulmonary contusion and the potential of resuscitation fluids to modulate this response.

Purpose of the Study:

  • To determine if pulmonary contusion primes the innate immune response in an animal model.
  • To test the hypothesis that resuscitation fluids can attenuate the primed immune response to a subsequent challenge.
  • To elucidate the role of Toll-like receptor 4 (TLR4) in this process.

Main Methods:

  • An animal model of pulmonary contusion was established in C57/BL6 mice.
  • Mice received a second hit via intratracheal lipopolysaccharide (LPS) administration 24 hours post-injury.
  • Experimental groups included injury + LPS, injury + vehicle, LPS alone, and injury followed by resuscitation with hypertonic saline (HTS) or Lactated Ringer's (LR) before LPS challenge.
  • Immune responses were assessed 4 hours after LPS challenge through analysis of blood, bronchoalveolar lavage fluid, and lung tissue.

Main Results:

  • Pulmonary contusion followed by LPS challenge resulted in immune priming, evidenced by increased lung injury, neutrophilia in bronchoalveolar lavage fluid, and elevated serum levels of IL-6, CXCL1, and MIP-2.
  • Compared to injury + vehicle or LPS alone, the injury + LPS group exhibited a significantly heightened inflammatory response.
  • Resuscitation with HTS, but not LR, effectively attenuated the primed immune response to the LPS challenge.

Conclusions:

  • Pulmonary contusion primes innate immunity, leading to an exaggerated response to a subsequent challenge with the TLR4 agonist, LPS.
  • Synergistic increases in inflammatory mediators and exacerbated lung injury were observed in injured animals challenged with LPS.
  • HTS resuscitation post-pulmonary contusion reduced the immune priming effect, suggesting a potential therapeutic benefit.