Kathelijne M Groeneveld1, Falco Hietbrink2, Timothy C Hardcastle3, Brian L Warren4, Leo Koenderman5, Luke P H Leenen6. 1. Department of Surgery, UMC Utrecht, The Netherlands. Electronic address: k.m.groeneveld@umcutrecht.nl. 2. Department of Surgery, UMC Utrecht, The Netherlands. Electronic address: f.hietbrink@hotmail.com. 3. Department of Surgery, Tygerberg Hospital, University of Stellenbosch, Cape Town, South Africa. Electronic address: timothyhar@ialch.co.za. 4. Department of Surgery, Tygerberg Hospital, University of Stellenbosch, Cape Town, South Africa. Electronic address: blw@sun.ac.za. 5. Department of Respiratory Medicine, UMC Utrecht, The Netherlands. Electronic address: l.koenderman@umcutrecht.nl. 6. Department of Surgery, UMC Utrecht, The Netherlands. Electronic address: l.p.h.leenen@umcutrecht.nl.
Abstract
INTRODUCTION: Trauma is one of the major causes of morbidity and mortality. Thoracic injuries are associated with inflammatory complications such as ARDS. The pathogenesis of this complication after pulmonary injury is incompletely understood, but neutrophils are thought to play a pivotal role. The aim of this project was to gain more insight in the role of thoracic injuries in the pathophysiological processes that link systemic neutrophil activation with inflammatory complications after trauma. METHODS: In this prospective cohort study fifty-five patients with isolated penetrating thoracic injury were included at a level one Trauma Unit. Blood samples were analysed for neutrophil phenotype with the use of flowcytometry within 3 h of trauma and repeated six and 24 h after injury. The presence of inflammatory complications (e.g. ARDS or sepsis/septic shock) was assessed during admission, and this was related to the neutrophil phenotpe. RESULTS: The clinical follow-up of fifty-three patients was uneventful. Only two patients developed an inflammatory complication. Within 3 h after trauma, neutrophils showed a decreased expression of FcγRII (p=0.007) and FcγRIII (p=0.001) compared to healthy individuals. After 6 h, expression of active FcγRII (p=0.017), C5aR (p=0.004) and CAECAM8 (p=0.043) increased, whereas L-selectin (p=0.002) decreased. After 24 h also CXCR-2 (CD182) expression increased compared to healthy individuals (p=0.001). CONCLUSIONS: Penetrating thoracic trauma leads to a distinct primed activation status of circulating neutrophils within hours. In addition to activation of cells, both young and reverse migrated neutrophils are released into the circulation. This degree of systemic inflammation does not exceed a threshold of inflammation that is needed for the development of inflammatory complications like ARDS.
INTRODUCTION:Trauma is one of the major causes of morbidity and mortality. Thoracic injuries are associated with inflammatory complications such as ARDS. The pathogenesis of this complication after pulmonary injury is incompletely understood, but neutrophils are thought to play a pivotal role. The aim of this project was to gain more insight in the role of thoracic injuries in the pathophysiological processes that link systemic neutrophil activation with inflammatory complications after trauma. METHODS: In this prospective cohort study fifty-five patients with isolated penetrating thoracic injury were included at a level one Trauma Unit. Blood samples were analysed for neutrophil phenotype with the use of flowcytometry within 3 h of trauma and repeated six and 24 h after injury. The presence of inflammatory complications (e.g. ARDS or sepsis/septic shock) was assessed during admission, and this was related to the neutrophil phenotpe. RESULTS: The clinical follow-up of fifty-three patients was uneventful. Only two patients developed an inflammatory complication. Within 3 h after trauma, neutrophils showed a decreased expression of FcγRII (p=0.007) and FcγRIII (p=0.001) compared to healthy individuals. After 6 h, expression of active FcγRII (p=0.017), C5aR (p=0.004) and CAECAM8 (p=0.043) increased, whereas L-selectin (p=0.002) decreased. After 24 h also CXCR-2 (CD182) expression increased compared to healthy individuals (p=0.001). CONCLUSIONS: Penetrating thoracic trauma leads to a distinct primed activation status of circulating neutrophils within hours. In addition to activation of cells, both young and reverse migrated neutrophils are released into the circulation. This degree of systemic inflammation does not exceed a threshold of inflammation that is needed for the development of inflammatory complications like ARDS.
Authors: B Relja; R Taraki; M P J Teuben; K Mörs; N Wagner; S Wutzler; F Hildebrand; M Perl; I Marzi Journal: BMC Pulm Med Date: 2016-12-01 Impact factor: 3.317
Authors: Esmaeil Mortaz; Seyed Sajjad Zadian; Mehri Shahir; Gert Folkerts; Johan Garssen; Sharon Mumby; Ian M Adcock Journal: Front Immunol Date: 2019-09-06 Impact factor: 7.561