TY - JOUR
T1 - Characteristics of inflammatory response and repair after experimental blast lung injury in rats
AU - Hamacher, Jürg
AU - Hadizamani, Yalda
AU - Huwer, Hanno
AU - Moehrlen, Ueli
AU - Bally, Lia
AU - Stammberger, Uz
AU - Wendel, Albrecht
AU - Lucas, Rudolf
N1 - Publisher Copyright:
© 2023 Hamacher et al.
PY - 2023/3
Y1 - 2023/3
N2 - 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.
AB - 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.
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U2 - 10.1371/journal.pone.0281446
DO - 10.1371/journal.pone.0281446
M3 - Article
C2 - 36928833
AN - SCOPUS:85150263045
SN - 1932-6203
VL - 18
JO - PloS one
JF - PloS one
IS - 3 March
M1 - e0281446
ER -