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

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.

[1]  M. Ushio-Fukai,et al.  Dichotomous Role of Tumor Necrosis Factor in Pulmonary Barrier Function and Alveolar Fluid Clearance , 2022, Frontiers in Physiology.

[2]  Yunen Liu,et al.  CD28 Deficiency Ameliorates Blast Exposure-Induced Lung Inflammation, Oxidative Stress, Apoptosis, and T Cell Accumulation in the Lungs via the PI3K/Akt/FoxO1 Signaling Pathway , 2019, Oxidative medicine and cellular longevity.

[3]  Mengyao Liu,et al.  Pathogenesis of Hypervirulent Group A Streptococcus. , 2018, Japan journal of medicine.

[4]  Jason E. Smith,et al.  Pathophysiology of primary blast injury , 2018, Journal of the Royal Army Medical Corps.

[5]  D. Männel,et al.  Cytokine–Ion Channel Interactions in Pulmonary Inflammation , 2018, Front. Immunol..

[6]  J. Wightman.  Pathophysiology of Primary Blast Injury. , 2017, Annals of emergency medicine.

[7]  A. Bull,et al.  CD43Lo classical monocytes participate in the cellular immune response to isolated primary blast lung injury , 2016, The journal of trauma and acute care surgery.

[8]  J. Clasper,et al.  What the Intensive Care Doctor Needs to Know about Blast-Related Lung Injury , 2013 .

[9]  D. Ma,et al.  Lung injury following lower extremity blast trauma in rats , 2012, The journal of trauma and acute care surgery.

[10]  M. Huber-Lang,et al.  Is the function of alveolar macrophages altered following blunt chest trauma? , 2011, Langenbeck's Archives of Surgery.

[11]  J. Catravas,et al.  Regulators of endothelial and epithelial barrier integrity and function in acute lung injury. , 2009, Biochemical pharmacology.

[12]  L. Kinzl,et al.  The pulmonary and hepatic immune microenvironment and its contribution to the early systemic inflammation following blunt chest trauma , 2006, Critical care medicine.

[13]  G. De Nucci,et al.  Inflammatory mechanisms underlying the rat pulmonary neutrophil influx induced by airway exposure to staphylococcal enterotoxin type A , 2005, British journal of pharmacology.

[14]  Akira Ohashi,et al.  Neutrophil depletion attenuates interleukin-8 production in mild-overstretch ventilated normal rabbit lung , 2004, Critical care medicine.

[15]  L. Kinzl,et al.  Induction of Apoptosis Following Blunt Chest Trauma , 2003, Shock.

[16]  E. E. Turk,et al.  Histologic, immunohistochemical, and ultrastructural findings in human blast lung injury. , 2003, American journal of respiratory and critical care medicine.

[17]  H. Uno,et al.  Change in location of cytokine-induced neutrophil chemoattractants (CINCs) in pulmonary silicosis. , 2003, Experimental and molecular pathology.

[18]  L. Kinzl,et al.  DOES BLUNT CHEST TRAUMA ALTER THE FUNCTION OF ALVEOLAR MACROPHAGES?: 42 , 2002 .

[19]  P. Suter,et al.  Tumor Necrosis Factor-α and Angiostatin Are Mediators of Endothelial Cytotoxicity in Bronchoalveolar Lavages of Patients with Acute Respiratory Distress Syndrome , 2002 .

[20]  M. Carraway,et al.  Extrinsic coagulation blockade attenuates lung injury and proinflammatory cytokine release after intratracheal lipopolysaccharide. , 2002, American journal of respiratory cell and molecular biology.

[21]  J. T. Owings,et al.  Injury induces increased monocyte expression of tissue factor: factors associated with head injury attenuate the injury-related monocyte expression of tissue factor. , 2002, The Journal of trauma.

[22]  S. Sauerland,et al.  Association between injury pattern of patients with multiple injuries and circulating levels of soluble tumor necrosis factor receptors, interleukin-6 and interleukin-10, and polymorphonuclear neutrophil elastase. , 2002, The Journal of trauma.

[23]  V. Castranova,et al.  Genistein prevents nuclear factor-kappa B activation and acute lung injury induced by lipopolysaccharide. , 2001, American journal of respiratory and critical care medicine.

[24]  M. Carraway,et al.  Tissue factor in experimental acute lung injury. , 2001, Seminars in hematology.

[25]  D. Edwards,et al.  Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-3 Are Key Regulators of Extracellular Matrix Degradation by Mouse Embryos1 , 2001, Biology of reproduction.

[26]  A. Wada,et al.  Role of cytokine-induced neutrophil chemoattractant-2 (CINC-2) alpha in a rat model of chronic bronchopulmonary infections with Pseudomonas aeruginosa. , 2000, Cytokine.

[27]  T. Akaike,et al.  Characteristic elevation of matrix metalloproteinase activity in idiopathic interstitial pneumonias. , 2000, American journal of respiratory and critical care medicine.

[28]  M. Gaxiola,et al.  Upregulation of gelatinases A and B, collagenases 1 and 2, and increased parenchymal cell death in COPD. , 2000, Chest.

[29]  T. Martin,et al.  Lung cytokines and ARDS: Roger S. Mitchell Lecture. , 1999, Chest.

[30]  Y. Ishii,et al.  Cytokine-Induced Neutrophil Chemoattractant in a Rat Model of Lipopolysaccharide-Induced Acute Lung Injury , 1999, Inflammation.

[31]  M. Jordana,et al.  IL-6 is an antiinflammatory cytokine required for controlling local or systemic acute inflammatory responses. , 1998, The Journal of clinical investigation.

[32]  P. Ward,et al.  Requirement for C-X-C chemokines (macrophage inflammatory protein-2 and cytokine-induced neutrophil chemoattractant) in IgG immune complex-induced lung injury. , 1997, Journal of immunology.

[33]  J. Lewtas,et al.  Role of endotoxin in tumor necrosis factor alpha expression from alveolar macrophages treated with urban air particles. , 1996, Experimental lung research.

[34]  S. Lowry,et al.  Biologic Control of Injury and Inflammation: Much More than Too Little or Too Late , 1996, World Journal of Surgery.

[35]  G. Žunić,et al.  Leukotrienes in the pathogenesis of pulmonary blast injury. , 1996, The Journal of trauma.

[36]  F. Stentz,et al.  Inflammatory cytokines in the BAL of patients with ARDS. Persistent elevation over time predicts poor outcome. , 1995, Chest.

[37]  G. Granger,et al.  Trauma causes sustained elevation of soluble tumor necrosis factor receptors. , 1994, Journal of the American College of Surgeons.

[38]  U. Steckholzer,et al.  Release of anti-inflammatory mediators after mechanical trauma correlates with severity of injury and clinical outcome. , 1994, The Journal of trauma.

[39]  P. De Baetselier,et al.  Mapping the lectin-like activity of tumor necrosis factor. , 1994, Science.

[40]  R. Sauerwein,et al.  Cytokine Patterns in Patients After Major Vascular Surgery, Hemorrhagic Shock, and Severe Blunt Trauma Relation with Subsequent Adult Respiratory Distress Syndrome and Multiple Organ Failure , 1993, Annals of surgery.

[41]  C A Smith,et al.  Soluble tumor necrosis factor (TNF) receptors are effective therapeutic agents in lethal endotoxemia and function simultaneously as both TNF carriers and TNF antagonists. , 1993, Journal of immunology.

[42]  L. R. Tan,et al.  Trauma causes early release of soluble receptors for tumor necrosis factor. , 1993, The Journal of trauma.

[43]  G. Murphy,et al.  Matrix metalloproteinases and their inhibitors. , 1992, Acta orthopaedica Scandinavica. Supplementum.

[44]  D. Wallach,et al.  Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors , 1992, The Journal of experimental medicine.

[45]  T. Mosmann,et al.  IL-10 inhibits cytokine production by activated macrophages. , 1991, Journal of immunology.

[46]  J. J. Thompson,et al.  Compartmentalization of intraalveolar and systemic lipopolysaccharide-induced tumor necrosis factor and the pulmonary inflammatory response. , 1989, The Journal of infectious diseases.

[47]  Explosions and Blast Injuries : A Primer for Clinicians , 2006 .

[48]  Kobi Peleg,et al.  Blast injuries. , 2005, The New England journal of medicine.

[49]  T. Keck,et al.  Matrix metalloproteinase-9 promotes neutrophil migration and alveolar capillary leakage in pancreatitis-associated lung injury in the rat. , 2002, Gastroenterology.

[50]  F. Gebhard,et al.  Untersuchungen zur systemischen posttraumatischen Inflammation in der Frühphase nach Trauma , 2000 .

[51]  M. Lerner,et al.  Global primary blast injury: a rat model. , 1998, The Journal of the Oklahoma State Medical Association.

[52]  U. Steckholzer,et al.  [Increased plasma level of Type I (p55) and Type II (p75) TNF-receptors following trauma]. , 1995, Swiss surgery = Schweizer Chirurgie = Chirurgie suisse = Chirurgia svizzera.

[53]  H. Tilg,et al.  Interleukin-6 (IL-6) as an anti-inflammatory cytokine: induction of circulating IL-1 receptor antagonist and soluble tumor necrosis factor receptor p55. , 1994, Blood.