Neutrophil-derived heparin binding protein—A mediator of increased vascular permeability after burns?

Johansson, Joakim; Lindbom, Lennart; Herwald, Heiko; Sjöberg, Folke

doi:10.1016/j.burns.2009.02.021

Cited by 17 publications

(17 citation statements)

References 15 publications

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“…In addition, we did not observe any difference in HBP between non-surviving and surviving sepsis patients. These observations are in line with two previous studies reporting that plasma levels of HBP did not correlate with the magnitude of tissue damage in burn patients [16] nor with the frequency of mortality in sepsis patients [17]. In this study, we found that patients with local infections, such as urinary tract infections, pneumonia and gastroenteritis without SIRS did not have higher levels of HBP compared to healthy controls.…”

Section: Discussionsupporting

confidence: 82%

Increased plasma levels of heparin-binding protein in patients with shock: a prospective, cohort study

et al. 2011

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Section: Discussionsupporting

confidence: 82%

Increased plasma levels of heparin-binding protein in patients with shock: a prospective, cohort study

et al. 2011

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“…However, antibodies which are found in TRALI have been shown to trigger discharge of azurocidin from neutrophils (192). In addition, in circumstances that may lead to ALI such as severe burns or sepsis, circulating azurocidin levels are increased significantly, allowing speculation on their potential role in lung damage (193)(194)(195).…”

Section: Neutrophil-derived Cationic Polypeptidesmentioning

confidence: 99%

Contribution of Neutrophils to Acute Lung Injury

Grommes

Soehnlein

2010

Mol Med

1,115

897

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Treatment of acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), remain unsolved problems of intensive care medicine. ALI/ARDS are characterized by lung edema due to increased permeability of the alveolar-capillary barrier and subsequent impairment of arterial oxygenation. Lung edema, endothelial and epithelial injury are accompanied by an influx of neutrophils into the interstitium and broncheoalveolar space. Hence, activation and recruitment of neutrophils are regarded to play a key role in progression of ALI/ARDS. Neutrophils are the first cells to be recruited to the site of inflammation and have a potent antimicrobial armour that includes oxidants, proteinases and cationic peptides. Under pathological circumstances, however, unregulated release of these microbicidal compounds into the extracellular space paradoxically can damage host tissues. This review focuses on the mechanisms of neutrophil recruitment into the lung and on the contribution of neutrophils to tissue damage in ALI.

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“…These injuries are associated with increased vascular permeability and edema formation. A study of 10 consecutive patients admitted to a burn unit showed that these patients had elevated HBP concentrations in plasma as compared to healthy controls [37] . HBP levels declined and reached almost normal levels within 24-48 h after the burn, known as the hyperpermeability phase, proposing a relationship between the HBP concentration in plasma and alterations in vascular permeability.…”

Section: Plasma Levels Of Hbp Are Increased In Severe Sepsismentioning

confidence: 99%

Roles of Heparin-Binding Protein in Bacterial Infections

2010

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Infectious diseases remain a major health problem, where sepsis and other severe infectious diseases are common causes of morbidity and mortality. The importance of early and appropriate treatment of sepsis and severe bacterial infections has been underlined by the successes of measures like the Surviving Sepsis Campaign, among others. Thus, there is a need for clinical and laboratory tools to identify a patient with severe infection early and to distinguish between bacterial and non-bacterial conditions. Heparin-binding protein (HBP) is also called azurocidin, or cationic antimicrobial protein of 37 kDa (CAP37). It is a multifunctional granule-associated protein that is rapidly mobilized from migrating polymorphonuclear leukocytes. HBP acts as a chemoattractant, an activator of monocytes and macrophages, and induces vascular leakage and edema formation. The release of HBP is triggered by ligation of neutrophilic β₂-integrins, a process that may be initiated by bacterial structures. The overall outcome is powerful vascular leakage. It has been shown that patients with severe sepsis express high levels of HBP in plasma before they develop hypotension. HBP is also involved in the pathophysiology of soft tissue infection. In conclusion, this protein is strongly involved in the pathophysiology of severe bacterial infections, and thus represents a potential diagnostic marker and a target for treatment.

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Neutrophil-derived heparin binding protein—A mediator of increased vascular permeability after burns?

Cited by 17 publications

References 15 publications

Increased plasma levels of heparin-binding protein in patients with shock: a prospective, cohort study

Increased plasma levels of heparin-binding protein in patients with shock: a prospective, cohort study

Contribution of Neutrophils to Acute Lung Injury

Roles of Heparin-Binding Protein in Bacterial Infections

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