Grimberg-Peters, Deborah, Bueren, Carina, Windolf, Joachim, Wahlers, Thorsten and Paunel-Goerguelue, Adnana (2016). Hyperbaric Oxygen Reduces Production of Reactive Oxygen Species in Neutrophils from Polytraumatized Patients Yielding in the Inhibition of p38 MAP Kinase and Downstream Pathways. PLoS One, 11 (8). SAN FRANCISCO: PUBLIC LIBRARY SCIENCE. ISSN 1932-6203

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Abstract

Trauma represents the leading cause of death among young people in western countries. Among the beneficial role of neutrophils in host defence, excessive priming and activation of neutrophils after major trauma lead to an overwhelming inflammatory response and secondary host tissue injury due to the release of toxic metabolites and enzymes. Hyperbaric oxygen (HBO) therapy has been proposed to possess antiinflammatory effects and might represent an appropriate therapeutic option to lower inflammation in a broad range of patients. Here, we studied the effects of HBO on the activity of neutrophils isolated from severely injured patients (days 1-2 after trauma), in fact on the production of reactive oxygen species (ROS) and release of neutrophil extracellular traps (NETs). We found exposure to HBO therapy to significantly diminish phorbol-12-myristate-13-acetate (PMA)-induced ROS production in neutrophils isolated from patients and healthy volunteers. At the same time, marked decrease in NETs release was found in control cells and a less pronounced reduction in patient neutrophils. Impaired ability to produce ROS following exposure to HBO was demonstrated to be linked to a strong downregulation of the activity of p38 MAPK. Only slight suppression of ERK activity could be found. In addition, HBO did not influence neutrophil chemotaxis or apoptosis, respectively. Collectively, this study shows for the first time that HBO therapy suppresses ROS production in inflammatory human neutrophils, and thus might impair ROS-dependent pathways, e.g. kinases activation and NETs release. Thus, HBO might represent a feasible therapy for patients suffering from systemic inflammation, including those with multiple trauma.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Grimberg-Peters, DeborahUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Bueren, CarinaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Windolf, JoachimUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Wahlers, ThorstenUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Paunel-Goerguelue, AdnanaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-266502
DOI: 10.1371/journal.pone.0161343
Journal or Publication Title: PLoS One
Volume: 11
Number: 8
Date: 2016
Publisher: PUBLIC LIBRARY SCIENCE
Place of Publication: SAN FRANCISCO
ISSN: 1932-6203
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
EXTRACELLULAR TRAPS; ACTIVATION; APOPTOSIS; CELLS; MCL-1; REPERFUSION; RECRUITMENT; RESISTANCE; EXPRESSION; NETOSISMultiple languages
Multidisciplinary SciencesMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/26650

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