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Published on: September 24, 2020
Club cell protein (CC)16 as potential lung injury marker in a porcine 72 h polytrauma model
Johannes Greven1, Jan Tilmann Vollrath2, Felix Bläsius1
1Department of Trauma and Reconstructive Surgery, RWTH Aachen University, Aachen, Germany.
Insights
Club cell protein (CC)16 shows promise as a lung injury biomarker in polytrauma patients. Early plasma and later bronchoalveolar lavage (BAL) CC16 levels may indicate lung damage in intensive care units (ICU).
Area of Science:
- Trauma research
- Biomarker discovery
- Pulmonology
Background:
- Thoracic trauma and polytrauma contribute significantly to mortality in severely injured patients.
- Lung complications like acute respiratory distress syndrome necessitate monitoring in intensive care units (ICUs).
- Club cell protein (CC)16, known for antioxidant properties, is emerging as a potential outcome-related biomarker.
Purpose of the Study:
- To evaluate club cell protein (CC)16 as a marker of lung damage.
- To investigate CC16's role in a porcine polytrauma model.
Main Methods:
- A 72-hour porcine polytrauma model including thoracic trauma, tibial fracture, hemorrhagic shock, and liver laceration was used.
- Blood plasma, bronchoalveolar lavage (BAL) fluid, and lung tissue samples were collected at various time points.
- ELISA was employed to measure CC16 and IL-8 concentrations, with histological analysis of ZO-1 and total protein content assessing lung tissue integrity and edema.
Main Results:
- Systemic CC16 levels were significantly elevated early after polytrauma compared to the sham group.
- Increased CC16 concentrations were observed in lung tissue and BAL fluid at 72 hours post-trauma.
- Elevated IL-8, total protein in BAL, and reduced ZO-1 staining indicated ongoing inflammation, barrier disruption, and edema in the trauma group.
Conclusions:
- This study provides the first evidence in a large animal polytrauma model that CC16 indicates lung damage.
- Both systemic and local CC16 responses are associated with lung injury.
- Early plasma and late BAL CC16 levels show potential as reliable markers for lung injury in polytrauma patients.
Background:
Polytrauma and respiratory tract damage after thoracic trauma cause about 25% of mortality among severely injured patients. Thoracic trauma can lead to the development of severe lung complications such as acute respiratory distress syndrome, and is, therefore, of great interest for monitoring in intensive care units (ICU). In recent years, club cell protein (CC)16 with its antioxidant properties has proven to be a potential outcome-related marker. In this study, we evaluated whether CC16 constitutes as a marker of lung damage in a porcine polytrauma model.
Methods:
In a 72 h ICU polytrauma pig model (thoracic trauma, tibial fracture, hemorrhagic shock, liver laceration), blood plasma samples (0, 3, 9, 24, 48, 72 h), BAL samples (72 h) and lung tissue (72 h) were collected. The trauma group (PT) was compared to a sham group. CC16 as a possible biomarker for lung injury in this model, and IL-8 concentrations as known indicator for ongoing inflammation during trauma were determined by ELISA. Histological analysis of ZO-1 and determination of total protein content were used to show barrier disruption and edema formation in lung tissue from the trauma group.
Results:
Systemic CC16 levels were significantly increased early after polytrauma compared vs. sham. After 72 h, CC16 concentration was significantly increased in lung tissue as well as in BAL in PT vs. sham. Similarly, IL-8 and total protein content in BAL were significantly increased in PT vs. sham. Evaluation of ZO-1 staining showed significantly lower signal intensity for polytrauma.
Conclusion:
The data confirm for the first time in a larger animal polytrauma model that lung damage was indicated by systemic and/or local CC16 response. Thus, early plasma and late BAL CC16 levels might be suitable to be used as markers of lung injury in this polytrauma model.

