| 1. |
- Herwald, Heiko, et al.
(författare)
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Foreword
- 2011
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Ingår i: Sepsis - Pro-Inflammatory and Anti-Inflammatory Responses : Good, Bad or Ugly? - Good, Bad or Ugly?. - Basel : KARGER. - 1662-291X .- 1420-9519. - 9783805597104 - 9783805597111 ; 17
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 2. |
- Agar, Cetin, et al.
(författare)
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beta(2)-Glycoprotein I: a novel component of innate immunity
- 2011
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Ingår i: Blood. - : American Society of Hematology. - 1528-0020 .- 0006-4971. ; 117:25, s. 6939-6947
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Tidskriftsartikel (refereegranskat)abstract
- Sepsis is a systemic host response to invasive infection by bacteria. Despite treatment with antibiotics, current mortality rates are in the range of 20%-25%, which makes sepsis the most important cause of death in intensive care. Gram-negative bacteria are a prominent cause of sepsis. Lipopolysaccharide (LPS), one of the major constituents of the outer membrane of Gram-negative bacteria, plays a major role in activating the host's immune response by binding to monocytes and other cells. Several proteins are involved in neutralization and clearance of LPS from the bloodstream. Here, we provide evidence that beta(2)-glycoprotein I (beta(2)GPI) is a scavenger of LPS. In vitro, beta(2)GPI inhibited LPS-induced expression of tissue factor and IL-6 from monocytes and endothelial cells. Binding of beta(2)GPI to LPS caused a conformational change in beta(2)GPI that led to binding of the beta(2)GPI-LPS complex to monocytes and ultimately clearance of this complex. Furthermore, plasma levels of beta(2)GPI were inversely correlated with temperature rise and the response of inflammatory markers after a bolus injection of LPS in healthy individuals. Together, these observations provide evidence that beta(2)GPI is involved in the neutralization and clearance of LPS and identify beta(2)GPI as a component of innate immunity. (Blood. 2011;117(25):6939-6947)
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| 3. |
- Beran, Ondrej, et al.
(författare)
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Heparin-binding protein as a biomarker of circulatory failure during severe infections: A report of three cases
- 2010
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Ingår i: Scandinavian Journal of Infectious Diseases. - : Informa UK Limited. - 1651-1980 .- 0036-5548. ; 42:8, s. 634-636
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- We report 3 cases of disease - leptospirosis, tropical malaria and fulminant meningococcaemia - associated with high serum concentrations of heparin-binding protein (HBP) and haemodynamic instability. Furthermore, HBP kinetics were observed for the first 3 days in survivors and were correlated with improvement in clinical condition.
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| 4. |
- Berkestedt, Ingrid, et al.
(författare)
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Elevated Plasma Levels of Antimicrobial Polypeptides in Patients with Severe Sepsis.
- 2010
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Ingår i: Journal of Innate Immunity. - : S. Karger AG. - 1662-811X .- 1662-8128. ; 2:5, s. 478-482
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Tidskriftsartikel (refereegranskat)abstract
- We wanted to investigate if plasma levels of antimicrobial polypeptides (AMPs) are increased in severe sepsis and if they correlate with severity and mortality. Samples were collected from 31 sepsis patients at the intensive care unit. The Sequential Organ Failure Assessment (SOFA) score and 90-day mortality were registered, and inflammatory markers and AMP levels were measured by ELISA. A median SOFA score (13) and cardiovascular SOFA score (3) indicated multiorgan failure with severe circulatory derangement, and elevated cytokine levels indicated inflammatory activation. Levels of bactericidal/permeability-increasing protein, heparin-binding protein, alpha-defensins and lactoferrin but not LL-37 were elevated in sepsis patients compared with controls. Bactericidal/permeability-increasing protein levels correlated with mortality, with lower levels in survivors. Levels of all AMPs, except LL-37, positively correlated with the cardiovascular SOFA score. In conclusion, levels of several AMPs are increased in sepsis and correlate with circulatory derangement. This probably reflects neutrophil activation as part of an innate immune response.
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| 5. |
- Blanchet, Xavier, et al.
(författare)
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Inflammatory role and prognostic value of platelet chemokines in acute coronary syndrome
- 2014
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Ingår i: Thrombosis and Haemostasis. - 0340-6245. ; 112:6, s. 1277-1287
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Tidskriftsartikel (refereegranskat)abstract
- Activated platelets and neutrophils exacerbate atherosclerosis. Platelets release the chemokines CXCL4, CXCL4L1 and CCL5, whereas myeloperoxidase (MPO) and azurocidin are neutrophil-derived. We investigated whether plasma levels of these platelet and neutrophil mediators are affected by the acute coronary syndrome (ACS), its medical treatment, concomitant clinical or laboratory parameters, and predictive for the progression of coronary artery disease (CAD). In an observational study, the association of various factors with plasma concentrations of platelet chemokines and neutrophil mediators in 204 patients, either upon admission with ACS and 6 hours later or without ACS or CAD, was determined by multiple linear regression. Mediator release was further analysed after activation of blood with ACS-associated triggers such as plaque material. CXCL4, CXCL4L1, CCL5, MPO and azurocidin levels were elevated in ACS. CXCL4 and CCL5 but not CXCL4L1 or MPO were associated with platelet counts and CRP. CXCL4 (in association with heparin treatment) and MPO declined over 6 hours during ACS. Elevated CCL5 was associated with a progression of CAD. Incubating blood with plaque material, PAR1 and PAR4 activation induced a marked release of CXCL4 and CCL5, whereas CXCL4L1 and MPO were hardly or not altered. Platelet chemokines and neutrophil products are concomitantly elevated in ACS and differentially modulated by heparin treatment. CCL5 levels during ACS predict a progression of preexisting CAD. Platelet-derived products appear to dominate the inflammatory response during ACS, adding to the emerging evidence that ACS per se may promote vascular inflammation.
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| 6. |
- Chalupa, P., et al.
(författare)
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Evaluation of potential biomarkers for the discrimination of bacterial and viral infections
- 2011
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Ingår i: Infection. - : Springer Science and Business Media LLC. - 1439-0973 .- 0300-8126. ; 39:5, s. 411-417
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Tidskriftsartikel (refereegranskat)abstract
- Purpose Timely knowledge of the bacterial etiology and localization of infection are important for empirical antibiotic therapy. Thus, the goal of this study was to evaluate routinely used biomarkers together with novel laboratory parameters in the diagnosis of infection. Methods In this prospective study, 54 adult patients with bacterial infections admitted to the Department of Infectious Diseases were included. For comparison, 27 patients with viral infections were enrolled. In these patients, white blood cell (WBC) counts, differential blood counts, serum levels of procalcitonin (PCT), IL-1 beta, IL-6, IL-8, IL-10, IL-12, TNF-alpha, IFN-gamma, soluble CD14 (sCD14), heparin-binding protein (HBP), cortisol (Cort), and monocyte surface expression of TLR2, TLR4, HLA-DR, and CD14 were analyzed. Also, these biomarkers were evaluated in 21 patients with acute community-acquired bacterial pneumonia (CABP), as well as in 21 patients with pyelonephritis and urosepsis. Results The highest sensitivity and specificity (expressed as the area under the curve [AUC]) for bacterial infection were observed in serum concentration of PCT (0.952), neutrophil and lymphocyte counts (0.852 and 0.841, respectively), and serumlevels of HBP (0.837), IL-6 (0.830), and Cort (0.817). In addition, the serum levels of IFN-gamma and Cort were significantly higher and IL-8 levels were lower in CABP when compared to pyelonephritis or urosepsis. Conclusions From the novel potential biomarkers, only PCT demonstrated superiority over the routine parameters in the differentiation of bacterial from viral infections. However, some of the novel parameters should be further evaluated in larger and better characterized cohorts of patients in order to find their clinical applications.
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| 7. |
- Chew, Michelle, et al.
(författare)
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Increased plasma levels of heparin-binding protein in patients with shock: a prospective, cohort study.
- 2012
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Ingår i: Inflammation Research. - : Springer Science and Business Media LLC. - 1420-908X .- 1023-3830. ; 61:4, s. 375-379
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Heparin-binding protein (HBP) is a potent inducer of increased vascular permeability. The purpose of this study was to examine plasma levels of HBP in patients with shock. DESIGN: Fifty-three consecutive patients with septic and non-septic shock at a mixed-bed intensive care unit were included, as well as 20 age-matched controls. Patients with local infections but without signs of shock served as infectious controls. Enzyme-linked immunosorbent assay was used to determine plasma levels of HBP. RESULTS: There were no differences in serum HBP levels between healthy controls and those with local infections, including urinary tract infections, pneumonia and gastroenteritis, without shock. Levels of HBP were higher in patients with non-septic shock and septic shock than healthy controls. However, there was no difference in serum HBP levels between patients with septic shock and those with non-septic shock. Moreover, HBP levels were not different between patients with low and high APACHE II scores. Plasma levels of HBP were similar in surviving and non-surviving patients with shock. CONCLUSIONS: HBP is elevated in patients with shock from septic and non-septic etiologies. Future investigations are required to define the functional role of HBP in patients with shock.
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