The journal of trauma and acute care surgery · 2026
Traumatic hemothorax activates complement, stimulates proinflammatory cytokine release, and primes neutrophils for local inflammatory reactive oxygen species production.
СтатьяНазвание и аннотация: Перевод в очереди
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Barmettler Nicolle K, White Collin M, Gawargi Flobater I, Maginot Elizabeth R, Moody Trace B, Sextro Kyle, Hiser Dylan, Clegg Ashely A, Hamed Mohamed, Tierney John F, Cantrell Emily, Lamb Gina D, Matos Miguel, Veatch Jessica, Moore Ernest E, Moore Hunter B, Moore Peter K, Bauman Zachary M, Henry Reynold, Barrett Christopher D
Аннотация
BACKGROUND: Traumatic hemothorax (HTX) is a frequent complication of chest wall injury, with ~300,000 cases annually in the United States. Pain often signifies underlying inflammation and may contribute to secondary complications after chest wall injury. We hypothesized that HTX leads to local, intrapleural complement activation and release of proinflammatory cytokines that can prime neutrophils for inflammatory reactive oxygen species (ROS) release.
METHODS: Adult trauma patients (N=15) with chest wall injury and HTX were consented for the study with IRB approval. HTX fluid and corresponding blood plasma were obtained in 3.2% citrate. Multiplex assays for complement analytes and proinflammatory cytokines were performed. Neutrophils from healthy donors were obtained and co-incubated with control platelet-poor plasma (PPP), trauma PPP, or corresponding HTX fluid and then challenged with vehicle control or N-formyl-methionyl-leucyl-phenylalanine (fMLP) in the presence of luminol, with ROS measured as luminescence over time. Pairwise comparisons were performed. Significance was set at p <0.05.
RESULTS: Compared with circulating trauma PPP, HTX fluid had significant local elevations of complement components Ba, C3a, C4a, and sC5b-9 (all p <0.01). Inflammatory cytokines showed a similar local elevation in HTX relative to trauma PPP, including TNF-alpha, IFN-gamma, IL-8, and MCP-1 (all p <0.05). Neutrophils did not generate significant ROS in response to healthy PPP, trauma PPP, or HTX in the absence of fMLP. When challenged with fMLP, HTX co-incubated neutrophils generated marked ROS that was significantly greater than trauma PPP co-incubated neutrophils ( p <0.05), demonstrating marked local neutrophil priming in HTX, while plasma co-incubated neutrophils were not primed for ROS generation.
CONCLUSIONS: Traumatic HTX is a highly inflammatory condition with locally enhanced complement activation, proinflammatory cytokine release, and inflammatory neutrophil priming for ROS production beyond that of circulating trauma plasma. Pain and secondary complications after chest wall injury with HTX may benefit from anti-inflammatory treatments in addition to pain control and drainage. ( J Trauma Acute Care Surg 2026;00:000-000. Copyright © 2026 Wolters Kluwer Health, Inc. All rights reserved.).
STUDY TYPE: Original Research.
LEVEL OF EVIDENCE: Basic Science; N/A.
METHODS: Adult trauma patients (N=15) with chest wall injury and HTX were consented for the study with IRB approval. HTX fluid and corresponding blood plasma were obtained in 3.2% citrate. Multiplex assays for complement analytes and proinflammatory cytokines were performed. Neutrophils from healthy donors were obtained and co-incubated with control platelet-poor plasma (PPP), trauma PPP, or corresponding HTX fluid and then challenged with vehicle control or N-formyl-methionyl-leucyl-phenylalanine (fMLP) in the presence of luminol, with ROS measured as luminescence over time. Pairwise comparisons were performed. Significance was set at p <0.05.
RESULTS: Compared with circulating trauma PPP, HTX fluid had significant local elevations of complement components Ba, C3a, C4a, and sC5b-9 (all p <0.01). Inflammatory cytokines showed a similar local elevation in HTX relative to trauma PPP, including TNF-alpha, IFN-gamma, IL-8, and MCP-1 (all p <0.05). Neutrophils did not generate significant ROS in response to healthy PPP, trauma PPP, or HTX in the absence of fMLP. When challenged with fMLP, HTX co-incubated neutrophils generated marked ROS that was significantly greater than trauma PPP co-incubated neutrophils ( p <0.05), demonstrating marked local neutrophil priming in HTX, while plasma co-incubated neutrophils were not primed for ROS generation.
CONCLUSIONS: Traumatic HTX is a highly inflammatory condition with locally enhanced complement activation, proinflammatory cytokine release, and inflammatory neutrophil priming for ROS production beyond that of circulating trauma plasma. Pain and secondary complications after chest wall injury with HTX may benefit from anti-inflammatory treatments in addition to pain control and drainage. ( J Trauma Acute Care Surg 2026;00:000-000. Copyright © 2026 Wolters Kluwer Health, Inc. All rights reserved.).
STUDY TYPE: Original Research.
LEVEL OF EVIDENCE: Basic Science; N/A.