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Neutrophil-derived heparin binding protein-A mediator of increased vascular permeability after burns?
Linköping University, Department of Medical and Health Sciences. Linköping University, Faculty of Health Sciences.
Karolinska Institute, Department Physiol and Pharmacol, Stockholm, Sweden .
Lund University, Department Clin Science, Div Infect Med, Lund, Sweden .
Linköping University, Department of Clinical and Experimental Medicine, Burn Center. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Reconstruction Centre, Department of Plastic Surgery, Hand surgery UHL.
2009 (English)In: BURNS, ISSN 0305-4179, Vol. 35, no 8, 1185-1187 p.Article in journal (Refereed) Published
Abstract [en]

Increased vascular permeability and oedema formation constitute a major clinical challenge following burns. Several clinical studies show that leukocytes are systemically activated following burns. Neutrophils have the capability to increase vascular permeability via mechanisms thought to involve the release of heparin binding protein (HBP). We hypothesised that HBP is elevated in plasma after major burns due to a systemic inflammatory response and investigated plasma-HBP concentrations in 10 severely burned patients daily for 1 week following the burn. Five-fold higher levels in plasma-HBP concentration compared to a control group were detected on the first day after injury, followed by a steep reduction in the time-period that corresponds to the last part of the hyperpermeability phase. These data are in accordance with the hypothesis that HBP may function as a mediator of the early bum-induced increase in vascular permeability, and call for further studies to confirm a possible cause-and-effect relationship between HBP and oedema formation following burns.

Place, publisher, year, edition, pages
2009. Vol. 35, no 8, 1185-1187 p.
Keyword [en]
Azurocidin, Burn, CAP-37, HBP, Trauma, Vascular permeability
National Category
Engineering and Technology
URN: urn:nbn:se:liu:diva-52834DOI: 10.1016/j.burns.2009.02.021OAI: diva2:285598
Available from: 2010-01-12 Created: 2010-01-12 Last updated: 2014-01-15Bibliographically approved
In thesis
1. Function of granulocytes after burns and trauma, associations with pulmonary vascular permeability, acute respiratory distress syndrome, and immunomodulation
Open this publication in new window or tab >>Function of granulocytes after burns and trauma, associations with pulmonary vascular permeability, acute respiratory distress syndrome, and immunomodulation
2013 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Background: Our innate immunesystem protects us from infections but, since its methods is not all specific for microorganisms, may also induce collateral damage.

Severe physical injury often proved deadly throughout evolution. Such injuries may induce massive collateral damage. Nowadays we can initiate advanced critical care for affected patients and save them from imminent trauma-related death. We are therefore faced with the fact that the collateral damage from the immune system may pose a major threat to the patient, the pathophysiology of which is not amenable to direct medical treatment and which leaves us with only passive supportive measures.

In this thesis we investigated the role of leucocytes under such circumstances.

Our main aim was to understand better the role of leucocytes in the development of increased vascular permeability after burns and trauma.

More specifically we investigated the impact of an injury on the function of leucocytes such as the dynamic change of certain cell-surface receptors on the leucocytes and in their numbers and immature forms. We wanted to find out if the increased pulmonary vascular permeability after a burn could be mediated through heparin binding protein (HBP) released from granuloctes, and whether HBP could be used as a biomarker for respiratory failure after trauma. We also wanted to confirm the possible role of histamine as a mediator of the systemic increase in vascular permeability after burns.

Methods: The dynamic change of cell-surface receptors was measured by flow-acquired cytometer scanning (FACS) on blood samples taken after burns. The concentrations of HBP after a burn and mechanical trauma were analysed in plasma. Pulmonary vascular permeability after a burn was assessed using transpulmonary thermodilution. The histamine turnover after a burn was assessed with high performance liquid chromatography (HPLC) for concentrations of histamine and methylhistamine in urine.

Results: We confirmed earlier investigations showing altered expression of receptors on leucocytes after a burn, receptors intimately associated with leucocyte functions (study I). In a pilot study of 10 patients we measured plasma concentrations of HBP and found them to be increased soon after a burn (study II). This finding was not confirmed in a larger, more extensive and specific study of 20 patients. We did, however, find an association between alterations in the number of leucocytes soon after a burn and pulmonary vascular permeability, indicating that they had a role in this process (study III).

In another study of trauma (non burn) we found an association between the concentration of HBP in early plasma-samples after injury and the development of ARDS, indicating that granulocytes and HBP have a role in its aetiology (study IV).

We found a small increase in urinary histamine and normal urinary methylhistamine concentrations but had anticipated a distinct increase followed by a decrease after reading the current papers on the subject. This indicates that the role of histamine as a mediator of increased vascular permeability after burns may have been exaggerated (study V).

Conclusions: We conclude that leucocytes are affected by burns and trauma, and it is likely that they contribute to the development of respiratory failure and acute respiratory distress syndrome (ARDS). HBP is a candidate biomarker for the early detection of ARDS after trauma, and the white blood count (WBC) is a useful biomarker for the detection of decreased oxygenation soon after a burn.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2013. 72 p.
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1362
ARDS, azurocidin, burn, CAP-37, critical care, granulocyte, HBP, histamine, intensive care, leucocyte, leukocyte, mediator, methylhistamine, MOF, oedema, neutrophil, permeability, PMN, trauma, vascular permeability
National Category
Medical and Health Sciences
urn:nbn:se:liu:diva-94513 (URN)978-91-7519-632-9 (print) (ISBN)
Public defence
2013-09-05, Elsa Brändström salen, Campus US, Linköpings universitet, Linköping, 09:00 (Swedish)
Available from: 2013-06-25 Created: 2013-06-25 Last updated: 2014-03-24Bibliographically approved

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Johansson, JoakimSjoberg, Folke
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Department of Medical and Health SciencesFaculty of Health SciencesBurn CenterDepartment of Plastic Surgery, Hand surgery UHL
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