The pathogenesis of pulmonary contusion: An open chest model in the rat

J. Jason Hoth, Joel D. Stitzel, F. Scott Gayzik, Noel A. Brownlee, Preston R. Miller, Barbara K. Yoza, Charles E. McCall, J. Wayne Meredith, R. Mark Payne

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

BACKGROUND: Chemokines direct leukocytes to areas of inflammation or injury. In general, CC chemokines (MCP-1, MIP-1α, RANTES) are chemoattractants for mononuclear cells and CXC (CINC-1, MIP-2α) for polymorphonuclear cells (PMNs). Herein we describe an open chest model of pulmonary contusion (PC) in a rodent (rat) and have identified a possible role for CC and CXC chemokines in the pathogenesis of PC. METHODS: Sprague-Dawley rats (350 g) underwent thoracotomy. The exposed lung was struck with a piston at 5.2 m/s (150 J/M). Blood, bronchoalveolar lavage (BAL), and lung tissue were collected at 3 hours and 24 hours after injury. PaO2/FiO2 (P/F) ratio was calculated at 15-minute intervals for 3 hours after contusion. Serum was evaluated for cytokine and chemokine expression using ELISA. Cell count/differential was performed on BAL, and lung tissue was obtained for histologic analysis, protein expression and wet to dry weights. Data are reported as pg/mL ± SE. Data were analyzed using Student's t test to identify significant differences (p ≤ 0.05 significant) between sham and injured animals. RESULTS: Piston impact caused PC based upon morphologic and histologic criteria. BAL cell count and lung wet to dry weights were increased and P/F ratio was decreased after PC. Systemic levels of IL-ra, MCP-1, and the CXC chemokines MIP-2α and CINC-1 were significantly elevated at 3 hours when sham and injured animals were compared. All chemokines were found to be significantly elevated at 24 hours, consistent with the early PMN and subsequent mononuclear infiltration observed in the contused lung. Pulmonary expression of TNF-α, IL-1β, CINC-1, MIP-2α, ICAM-1, and elastase were increased and activated systemic neutrophils showed increased CD-11b. CONCLUSION: A model of PC is described in which innate inflammation is activated locally and systemically. Systemic levels of CC and CXC chemokines are increased after PC. This correlates with elevated PMN CD-11b expression, enhanced pulmonary ICAM-1 expression, and mononuclear and PMN infiltration into the lung and alveolar space. Elevated levels of CC and CXC chemokines are seen after PC and may be involved in the lung's inflammatory response to injury.

Original languageEnglish (US)
Pages (from-to)32-44
Number of pages13
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume61
Issue number1
DOIs
StatePublished - Jul 1 2006

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Contusions
Thorax
Lung
CXC Chemokines
CC Chemokines
Bronchoalveolar Lavage
Chemokines
Intercellular Adhesion Molecule-1
Wounds and Injuries
Cell Count
Inflammation
Weights and Measures
Chemokine CCL5
Pancreatic Elastase
Chemotactic Factors
Pulmonary Edema
Thoracotomy
Interleukin-1
Sprague Dawley Rats

Keywords

  • Chemokines
  • Inflammation
  • Innate immunity
  • Pulmonary contusion
  • Rodent model
  • Trauma

ASJC Scopus subject areas

  • Surgery

Cite this

The pathogenesis of pulmonary contusion : An open chest model in the rat. / Hoth, J. Jason; Stitzel, Joel D.; Gayzik, F. Scott; Brownlee, Noel A.; Miller, Preston R.; Yoza, Barbara K.; McCall, Charles E.; Meredith, J. Wayne; Payne, R. Mark.

In: Journal of Trauma - Injury, Infection and Critical Care, Vol. 61, No. 1, 01.07.2006, p. 32-44.

Research output: Contribution to journalArticle

Hoth, JJ, Stitzel, JD, Gayzik, FS, Brownlee, NA, Miller, PR, Yoza, BK, McCall, CE, Meredith, JW & Payne, RM 2006, 'The pathogenesis of pulmonary contusion: An open chest model in the rat', Journal of Trauma - Injury, Infection and Critical Care, vol. 61, no. 1, pp. 32-44. https://doi.org/10.1097/01.ta.0000224141.69216.aa
Hoth, J. Jason ; Stitzel, Joel D. ; Gayzik, F. Scott ; Brownlee, Noel A. ; Miller, Preston R. ; Yoza, Barbara K. ; McCall, Charles E. ; Meredith, J. Wayne ; Payne, R. Mark. / The pathogenesis of pulmonary contusion : An open chest model in the rat. In: Journal of Trauma - Injury, Infection and Critical Care. 2006 ; Vol. 61, No. 1. pp. 32-44.
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abstract = "BACKGROUND: Chemokines direct leukocytes to areas of inflammation or injury. In general, CC chemokines (MCP-1, MIP-1α, RANTES) are chemoattractants for mononuclear cells and CXC (CINC-1, MIP-2α) for polymorphonuclear cells (PMNs). Herein we describe an open chest model of pulmonary contusion (PC) in a rodent (rat) and have identified a possible role for CC and CXC chemokines in the pathogenesis of PC. METHODS: Sprague-Dawley rats (350 g) underwent thoracotomy. The exposed lung was struck with a piston at 5.2 m/s (150 J/M). Blood, bronchoalveolar lavage (BAL), and lung tissue were collected at 3 hours and 24 hours after injury. PaO2/FiO2 (P/F) ratio was calculated at 15-minute intervals for 3 hours after contusion. Serum was evaluated for cytokine and chemokine expression using ELISA. Cell count/differential was performed on BAL, and lung tissue was obtained for histologic analysis, protein expression and wet to dry weights. Data are reported as pg/mL ± SE. Data were analyzed using Student's t test to identify significant differences (p ≤ 0.05 significant) between sham and injured animals. RESULTS: Piston impact caused PC based upon morphologic and histologic criteria. BAL cell count and lung wet to dry weights were increased and P/F ratio was decreased after PC. Systemic levels of IL-ra, MCP-1, and the CXC chemokines MIP-2α and CINC-1 were significantly elevated at 3 hours when sham and injured animals were compared. All chemokines were found to be significantly elevated at 24 hours, consistent with the early PMN and subsequent mononuclear infiltration observed in the contused lung. Pulmonary expression of TNF-α, IL-1β, CINC-1, MIP-2α, ICAM-1, and elastase were increased and activated systemic neutrophils showed increased CD-11b. CONCLUSION: A model of PC is described in which innate inflammation is activated locally and systemically. Systemic levels of CC and CXC chemokines are increased after PC. This correlates with elevated PMN CD-11b expression, enhanced pulmonary ICAM-1 expression, and mononuclear and PMN infiltration into the lung and alveolar space. Elevated levels of CC and CXC chemokines are seen after PC and may be involved in the lung's inflammatory response to injury.",
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T1 - The pathogenesis of pulmonary contusion

T2 - An open chest model in the rat

AU - Hoth, J. Jason

AU - Stitzel, Joel D.

AU - Gayzik, F. Scott

AU - Brownlee, Noel A.

AU - Miller, Preston R.

AU - Yoza, Barbara K.

AU - McCall, Charles E.

AU - Meredith, J. Wayne

AU - Payne, R. Mark

PY - 2006/7/1

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N2 - BACKGROUND: Chemokines direct leukocytes to areas of inflammation or injury. In general, CC chemokines (MCP-1, MIP-1α, RANTES) are chemoattractants for mononuclear cells and CXC (CINC-1, MIP-2α) for polymorphonuclear cells (PMNs). Herein we describe an open chest model of pulmonary contusion (PC) in a rodent (rat) and have identified a possible role for CC and CXC chemokines in the pathogenesis of PC. METHODS: Sprague-Dawley rats (350 g) underwent thoracotomy. The exposed lung was struck with a piston at 5.2 m/s (150 J/M). Blood, bronchoalveolar lavage (BAL), and lung tissue were collected at 3 hours and 24 hours after injury. PaO2/FiO2 (P/F) ratio was calculated at 15-minute intervals for 3 hours after contusion. Serum was evaluated for cytokine and chemokine expression using ELISA. Cell count/differential was performed on BAL, and lung tissue was obtained for histologic analysis, protein expression and wet to dry weights. Data are reported as pg/mL ± SE. Data were analyzed using Student's t test to identify significant differences (p ≤ 0.05 significant) between sham and injured animals. RESULTS: Piston impact caused PC based upon morphologic and histologic criteria. BAL cell count and lung wet to dry weights were increased and P/F ratio was decreased after PC. Systemic levels of IL-ra, MCP-1, and the CXC chemokines MIP-2α and CINC-1 were significantly elevated at 3 hours when sham and injured animals were compared. All chemokines were found to be significantly elevated at 24 hours, consistent with the early PMN and subsequent mononuclear infiltration observed in the contused lung. Pulmonary expression of TNF-α, IL-1β, CINC-1, MIP-2α, ICAM-1, and elastase were increased and activated systemic neutrophils showed increased CD-11b. CONCLUSION: A model of PC is described in which innate inflammation is activated locally and systemically. Systemic levels of CC and CXC chemokines are increased after PC. This correlates with elevated PMN CD-11b expression, enhanced pulmonary ICAM-1 expression, and mononuclear and PMN infiltration into the lung and alveolar space. Elevated levels of CC and CXC chemokines are seen after PC and may be involved in the lung's inflammatory response to injury.

AB - BACKGROUND: Chemokines direct leukocytes to areas of inflammation or injury. In general, CC chemokines (MCP-1, MIP-1α, RANTES) are chemoattractants for mononuclear cells and CXC (CINC-1, MIP-2α) for polymorphonuclear cells (PMNs). Herein we describe an open chest model of pulmonary contusion (PC) in a rodent (rat) and have identified a possible role for CC and CXC chemokines in the pathogenesis of PC. METHODS: Sprague-Dawley rats (350 g) underwent thoracotomy. The exposed lung was struck with a piston at 5.2 m/s (150 J/M). Blood, bronchoalveolar lavage (BAL), and lung tissue were collected at 3 hours and 24 hours after injury. PaO2/FiO2 (P/F) ratio was calculated at 15-minute intervals for 3 hours after contusion. Serum was evaluated for cytokine and chemokine expression using ELISA. Cell count/differential was performed on BAL, and lung tissue was obtained for histologic analysis, protein expression and wet to dry weights. Data are reported as pg/mL ± SE. Data were analyzed using Student's t test to identify significant differences (p ≤ 0.05 significant) between sham and injured animals. RESULTS: Piston impact caused PC based upon morphologic and histologic criteria. BAL cell count and lung wet to dry weights were increased and P/F ratio was decreased after PC. Systemic levels of IL-ra, MCP-1, and the CXC chemokines MIP-2α and CINC-1 were significantly elevated at 3 hours when sham and injured animals were compared. All chemokines were found to be significantly elevated at 24 hours, consistent with the early PMN and subsequent mononuclear infiltration observed in the contused lung. Pulmonary expression of TNF-α, IL-1β, CINC-1, MIP-2α, ICAM-1, and elastase were increased and activated systemic neutrophils showed increased CD-11b. CONCLUSION: A model of PC is described in which innate inflammation is activated locally and systemically. Systemic levels of CC and CXC chemokines are increased after PC. This correlates with elevated PMN CD-11b expression, enhanced pulmonary ICAM-1 expression, and mononuclear and PMN infiltration into the lung and alveolar space. Elevated levels of CC and CXC chemokines are seen after PC and may be involved in the lung's inflammatory response to injury.

KW - Chemokines

KW - Inflammation

KW - Innate immunity

KW - Pulmonary contusion

KW - Rodent model

KW - Trauma

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