Enhanced neutrophil migratory activity following major blunt trauma

Bhatia, R.; Pallister, Ian; Dent, Chris; Jones, Simon A.; Topley, Nicholas

doi:10.1016/j.injury.2005.03.009

Cited by 37 publications

(44 citation statements)

References 26 publications

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“…The development of pulmonary complications after trauma has been closely associated with an excessive systemic and local immune reaction [13,48,49]. This complex immune response to trauma is characterized by the release of several inflammatory mediators including IL-8, IL-1β, IL-10 and IL-18 but also neutrophil migration into the lung [13,[48][49][50][51][52][53].…”

Section: Discussionmentioning

confidence: 99%

“…This complex immune response to trauma is characterized by the release of several inflammatory mediators including IL-8, IL-1β, IL-10 and IL-18 but also neutrophil migration into the lung [13,[48][49][50][51][52][53]. Persistent accumulation of neutrophils in the lung has been linked to pulmonary damage and poor survival via an interstitial inflammation, increase of interstitial space and limitation of the oxygen transport [9][10][11][12].…”

Section: Discussionmentioning

confidence: 99%

“…4 and 5). As rationale for an increased neutrophil accumulation via IL-8, it has been demonstrated that IL-8 might be directly involved in post-traumatic pulmonary inflammatory processes by attracting PMN to the lung [13]. More recently, it has been shown that down-regulating the surface expression of the IL-8 receptors CXCR1/2 significantly blocked IL-8-induced neutrophil migration in vitro and in vivo in a model of pulmonary inflammation [29].…”

Section: Discussionmentioning

confidence: 99%

“…interleukin (IL)−8 into the pulmonary interstitium, release proteolytic enzymes and induce microvascular damage and harmful airway remodeling in lung tissue, which is associated with poor survival [9][10][11][12]. Moreover, the generation of inflammatory mediators including interleukin IL-8 plays an important role in ARDS pathophysiology [13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

“…But it may assumed that IL-8 as well as LTB4 might be directly involved in post-traumatic pulmonary inflammatory processes by attracting PMN to the lung [13,27]. This is considered as one of the main factors of interstitial inflammation in the lungs, extending the transport distance for gas exchange.…”

Section: Introductionmentioning

confidence: 99%

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Leukotriene B4 indicates lung injury and on-going inflammatory changes after severe trauma in a porcine long-term model

Störmann

Auner

Schimunek

et al. 2017

Prostaglandins, Leukotrienes and Essential Fatty Acids

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A B S T R A C TBackground: Recognizing patients at risk for pulmonary complications (PC) is of high clinical relevance. Migration of polymorphonuclear leukocytes (PMN) to inflammatory sites plays an important role in PC, and is tightly regulated by specific chemokines including interleukin (IL)−8 and other mediators such as leukotriene (LT)B4. Previously, we have reported that LTB4 indicated early patients at risk for PC after trauma. Here, the relevance of LTB4 to indicating lung integrity in a newly established long-term porcine severe trauma model (polytrauma, PT) was explored. Methods: Twelve pigs (3 months old, 30 ± 5 kg) underwent PT including standardized femur fracture, lung contusion, liver laceration, hemorrhagic shock, subsequent resuscitation and surgical fracture fixation. Six animals served as controls (sham). After 72 h lung damage and inflammatory changes were assessed. LTB4 was determined in plasma before the experiment, immediately after trauma, and after 2, 4, 24 or 72 h. Bronchoalveolar lavage (BAL)-fluid was collected prior and after the experiment. Results: Lung injury, local gene expression of IL-8, IL-1β, IL-10, IL-18 and PMN-infiltration into lungs increased significantly in PT compared with sham. Systemic LTB4 increased markedly in both groups 4 h after trauma. Compared with declined plasma LTB4 levels in sham, LTB4 increased further in PT after 72 h. Similar increase was observed in BAL-fluid after PT. Conclusions: In a severe trauma model, sustained changes in terms of lung injury and inflammation are determined at day 3 post-trauma. Specifically, increased LTB4 in this porcine long-term model indicated a rapid inflammatory alteration both locally and systemically. The results support the concept of LTB4 as a biomarker for PC after severe trauma and lung contusion.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Leukotriene B4 indicates lung injury and on-going inflammatory changes after severe trauma in a porcine long-term model

Störmann

Auner

Schimunek

et al. 2017

Prostaglandins, Leukotrienes and Essential Fatty Acids

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Contributing factors in the development of acute lung injury in a murine double hit model

Störmann

Becker

Künnemeyer

et al. 2019

Eur J Trauma Emerg Surg

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Standardized porcine unilateral femoral nailing is associated with changes in PMN activation status, rather than aberrant systemic PMN prevalence

Teuben

Pfeifer²,

Horst

et al. 2021

Eur J Trauma Emerg Surg

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Purpose Intramedullary nailing (IMN) of fractures is associated with increased rates of inflammatory complications. The pathological mechanism underlying this phenomenon is unclear. However, polymorphonuclear granulocytes (PMNs) seem to play an important role. We hypothesized that a femur fracture and standardized IMN in pigs is associated with altered appearance of PMNs in circulation and enhanced activation status of these cells. Methods A porcine model including a femur fracture and IMN was utilized. Animals were randomized for control [anesthesia + mechanical ventilation only (A/MV)] and intervention [A/MV and unilateral femur fracture (FF) + IMN] conditions. PMN numbers and responsiveness, integrin (CD11b), L-selectin (CD62L) and Fcγ-receptor (CD16 and CD32)-expression levels were measured by flowcytometry of blood samples. Animals were observed for 72 h. Results Circulatory PMN numbers did not differ between groups. Early PMN-responsiveness was retained after insult. PMN-CD11b expression increased significantly upon insult and peaked after 24 h, whereas CD11b in control animals remained unaltered (P = 0.016). PMN-CD16 expression levels in the FF + IMN-group rose gradually over time and were significantly higher compared with control animals, after 48 h (P = 0.016) and 72 h (P = 0.032). PMN-CD62L and CD32 expression did not differ significantly between conditions. Conclusion This study reveals that a femur fracture and subsequent IMN in a controlled setting in pigs is associated with enhanced activation status of circulatory PMNs, preserved PMN-responsiveness and unaltered circulatory PMN-presence. Indicating that monotrauma plus IMN is a specific and substantial stimulus for the cellular immune system. Early alterations of circulatory PMN receptor expression dynamics may be predictive for the intensity of the post traumatic response.

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Enhanced neutrophil migratory activity following major blunt trauma

Cited by 37 publications

References 26 publications

Leukotriene B4 indicates lung injury and on-going inflammatory changes after severe trauma in a porcine long-term model

Leukotriene B4 indicates lung injury and on-going inflammatory changes after severe trauma in a porcine long-term model

Contributing factors in the development of acute lung injury in a murine double hit model

Standardized porcine unilateral femoral nailing is associated with changes in PMN activation status, rather than aberrant systemic PMN prevalence

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