Heparin-Binding Protein Decreases Apoptosis in Human and Murine Neutrophils

Shrotri, M; Kuhn, John F; Peyton, James C.; Flodgaard, Hans; Klein, Jon B.; Cheadle, William G.

doi:10.1006/jsre.1999.5803

Cited by 6 publications

(2 citation statements)

References 30 publications

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“…Colony stimulating factors (CSF), IL-6, IL-8, glucocorticoids, heparin-binding protein, endotoxin, and even leukocyte elective surgery and thermal injury are known to delay apoptosis (29)(30)(31)(32)(33)(34)(35). Conversely, anti-inflammatory cytokines, such as IL-10, accelerate the apoptosis of LPSactivated neutrophils (36).…”

Section: Discussionmentioning

confidence: 99%

Endotoxin Inhibits Apoptosis but Induces Primary Necrosis in Neutrophils

et al. 2005

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Lipopolysaccharide (LPS) is known to prolong the functional lifespan of neutrophils at a site of infection by preventing apoptosis through inhibitor of apoptosis proteins (IAPs). We hypothesized that the increased neutrophil lifespan ultimately leads to a larger fraction of cells undergoing uncontrolled, primary necrosis. Diluted venous whole blood was incubated with increasing concentrations of LPS for up to 36 hr. The percentages of apoptotic, necrotic and viable neutrophils were assessed using the Annexin V/propidium iodide flow cytometric assay. LPS led to a reduction of neutrophil apoptosis and increased the number of viable cells at 12, 24, and 36 hr of incubation. At the same time intervals, there was a significant increase in the percentage of cells undergoing primary necrosis for all concentrations of LPS (e.g., 10 ng/ml LPS at 24 h produced a mean increase from 9.6% in controls to 30.6%, p < 0.001). This increase in direct neutrophil necrosis following LPS activation may amplify local proinflammatory effects through less well controlled release of neutrophil contents into surrounding tissue.

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Section: Discussionmentioning

confidence: 99%

Endotoxin Inhibits Apoptosis but Induces Primary Necrosis in Neutrophils

et al. 2005

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“…Nevertheless, another study showed that HBP levels did not correlate with survival in nonseptic and septic shock patients [24]. HBP has been shown to increase the survival of cultured monocytes and protect them from oxidative stress [4,26]. HBP-treated endothelial cells also demonstrated enhanced survival in apoptosis assays, suggesting that HBP may play a protective role during an inflammatory response [27].…”

Section: Discussionmentioning

confidence: 99%

Increased plasma levels of heparin-binding protein in patients with acute respiratory distress syndrome

Lin

Shen

et al. 2013

Crit Care

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IntroductionHeparin-binding protein (HBP) is an antimicrobial protein stored in neutrophil granules and plays a role in endothelial permeability regulation. The aim was to assess the diagnostic and prognostic value of measuring HBP in patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS).MethodsPlasma HBP was collected from 78 patients with ALI/ARDS, 28 patients with cardiogenic pulmonary edema (CPE) and 20 healthy volunteers at enrollment. Levels of HBP were measured by ELISA.ResultsPatients with ALI/ARDS had significantly higher median levels of HBP compared with patients with CPE (17.15 (11.95 to 24.07) ng/ml vs. 9.50 (7.98 to 12.18) ng/ml, P <0.001) at enrollment. There was no significant difference between CPE patients and healthy subjects in terms of HBP value (P = 0.372). The HBP levels of nonsurvivors was significantly higher than that of survivors (23.90 (14.81 to 32.45) ng/ml vs. 16.01 (10.97 to 21.06) ng/ml, P = 0.012) and multivariate logistic regression showed HBP (odds ratio =1.52, P = 0.034) was the independent predictor for 30-day mortality in patients with ALI/ARDS.ConclusionsPlasma HBP levels of ALI/ARDS patients were significantly higher than that of CPE patients. HBP was a strong prognostic marker for short-term mortality in ALI/ARDS.

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