Characteristics of inflammatory response and repair after experimental blast lung injury in rats

PLoS One. 2023 Mar 16;18(3):e0281446. doi: 10.1371/journal.pone.0281446. eCollection 2023.

Abstract

Background and objectives: Blast-induced lung injury is associated with inflammatory, which are characterised by disruption of the alveolar-capillary barrier, haemorrhage, pulmonary infiltrateration causing oedema formation, pro-inflammatory cytokine and chemokine release, and anti-inflammatory counter-regulation. The objective of the current study was to define sequence of such alterations in with establishing blast-induced lung injury in rats using an advanced blast generator.

Methods: Rats underwent a standardized blast wave trauma and were euthanised at defined time points. Non-traumatised animals served as sham controls. Obtained samples from bronchoalveolar lavage fluid (BALF) at each time-point were assessed for histology, leukocyte infiltration and cytokine/chemokine profile.

Results: After blast lung injury, significant haemorrhage and neutrophil infiltration were observed. Similarly, protein accumulation, lactate dehydrogenase activity (LDH), alveolar eicosanoid release, matrix metalloproteinase (MMP)-2 and -9, pro-Inflammatory cytokines, including tumour necrosis factor (TNF) and interleukin (IL) -6 raised up. While declining in the level of anti-inflammatory cytokine IL-10 occurred. Ultimately, pulmonary oedema developed that increased to its maximum level within the first 1.5 h, then recovered within 24 h.

Conclusion: Using a stablished model, can facilitate the study of inflammatory response to blast lung injury. Following the blast injury, alteration in cytokine/chemokine profile and activity of cells in the alveolar space occurs, which eventuates in alveolar epithelial barrier dysfunction and oedema formation. Most of these parameters exhibit time-dependent return to their basal status that is an indication to resilience of lungs to blast-induced lung injury.

MeSH terms

  • Animals
  • Cytokines
  • Edema
  • Interleukin-6
  • Lung / metabolism
  • Lung Injury* / etiology
  • Pulmonary Edema*
  • Rats
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Cytokines
  • Tumor Necrosis Factor-alpha
  • Interleukin-6

Grants and funding

The author(s) received no specific funding for this work.