S S Frøland

Oslo University Hospital, Kristiania (historical), Oslo County, Norway

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Publications (299)1358.69 Total impact

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    ABSTRACT: Despite recent advances in microbiological techniques, the etiology of community-acquired pneumonia (CAP) is still not well described. We applied polymerase chain reaction (PCR) and conventional methods to describe etiology of CAP in hospitalized adults and evaluated their respective diagnostic yields. 267 CAP patients were enrolled consecutively over our 3-year prospective study. Conventional methods (i.e., bacterial cultures, urinary antigen assays, serology) were combined with nasopharyngeal (NP) and oropharyngeal (OP) swab samples analyzed by real-time quantitative PCR (qPCR) for Streptococcus pneumoniae, and by real-time PCR for Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bordetella pertussis and 12 types of respiratory viruses. Etiology was established in 167 (63%) patients with 69 (26%) patients having ≥1 copathogen. There were 75 (28%) pure bacterial and 41 (15%) pure viral infections, and 51 (19%) viral-bacterial coinfections, resulting in 126 (47%) patients with bacterial and 92 (34%) patients with viral etiology. S. pneumoniae (30%), influenza (15%) and rhinovirus (12%) were most commonly identified, typically with ≥1 copathogen. During winter and spring, viruses were detected more frequently (45%, P=.01) and usually in combination with bacteria (39%). PCR improved diagnostic yield by 8% in 64 cases with complete sampling (and by 15% in all patients); 5% for detection of bacteria; 19% for viruses (P=.04); and 16% for detection of ≥1 copathogen. Etiology was established in 79% of 43 antibiotic-naive patients with complete sampling. S. pneumoniae qPCR positive rate was significantly higher for OP swab compared to NP swab (P<.001). Positive rates for serology were significantly higher than for real-time PCR in detecting B. pertussis (P=.001) and influenza viruses (P<.001). Etiology could be established in 4 out of 5 CAP patients with the aid of PCR, particularly in diagnosing viral infections. S. pneumoniae and viruses were most frequently identified, usually with copathogens. Viral-bacterial coinfections were more common than pure infections during winter and spring; a finding we consider important in the proper management of CAP. When swabbing for qPCR detection of S. pneumoniae in adult CAP, OP appeared superior to NP, but this finding needs further confirmation. ClinicalTrials.gov Identifier: NCT01563315 .
    BMC Infectious Diseases 12/2015; 15(1). DOI:10.1186/s12879-015-0803-5 · 2.56 Impact Factor
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    ABSTRACT: Patients with common variable immunodeficiency (CVID) have reduced numbers and frequencies of dendritic cells (DCs) in blood, and there is also evidence for defective activation through toll-like receptors (TLRs). Collectively, these observations may point to a primary defect in the generation of functional DCs. Here, we measured frequencies of plasmacytoid DCs (pDCs) and myeloid DCs (mDCs) in peripheral blood of 26 CVID patients and 16 healthy controls. The results show that the patients have reduced absolute counts of both subsets. However, the decreased numbers in peripheral blood were not reflected in reduced frequencies of CD34(+) pDC progenitors in the bone marrow. Moreover, studies at the single cell level showed that DCs from CVID patients and healthy controls produced similar amounts of interferon-α or interleukin-12 and expressed similar levels of activation markers in response to human cytomegalovirus and ligands for TLR7 and TLR9. The study represents the most thorough functional characterization to date, and the first to assess bone marrow progenitor output, of naturally occurring DCs in CVID. In conclusion, it seems unlikely that CVID is secondary to insufficient production of naturally occurring DCs or a defect in their signalling through TLR7 or TLR9.
    Clinical & Experimental Immunology 11/2013; DOI:10.1111/cei.12239 · 3.28 Impact Factor
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    ABSTRACT: Introduction. Besides hypogammaglobulinemia and recurrent infections, abnormalities of T-cells might contribute to lung damage in common variable immunodeficiency disorders (CVID). Materials and methods. In 16 adult patients, the majority of whom had pulmonary abnormalities, we studied T-cell subsets and markers of inflammation in bronchoalveolar lavage fluid (BALF) and blood and their relations with pulmonary function and high resolution computed tomography (HRCT). Results. We demonstrated that some of the lymphocyte abnormalities previously demonstrated in peripheral blood from CVID patients, such as low CD4/CD8 T-cell ratio, were also present in BALF. Moreover, low BALF CD4/CD8 ratio (≤ 1), found in seven patients, was significantly associated with higher blood CD8(+) cell count and to lower values of the lung function variables; forced expiratory volume (FVC), total lung capacity (TLC), vital capacity (VC) and residual volume (RV) in % of predicted. The expression of the inflammatory markers HLA-DR and CCR5 on T-cells was significantly higher, and the expression of CCR7 significantly lower, in BALF compared to blood, possibly reflecting an inflammatory/cytotoxic T-cell phenotype within pulmonary tissue in CVID. Furthermore, patients with bronchiectasis had higher concentrations of the pro-inflammatory cytokine TNFα in plasma, compared to those without. Conclusion. Our findings suggest that inflammation and T-cell activation may be involved in the immunopathogenesis of pulmonary complications in CVID.
    Scandinavian journal of clinical and laboratory investigation 08/2013; DOI:10.3109/00365513.2013.819523 · 1.38 Impact Factor
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    ABSTRACT: Background: New drugs for rheumatoid arthritis (RA) have resulted in an improvement in patients' functioning and morbidity, but are linked with increased risk of infections. Traditional immunosuppressant drugs are often used in combination with anti-tumour necrosis factor-alpha (TNF-ɑ) inhibitors or anti-CD20 (rituximab). Method: The review is based on a search in PubMed and on the authors' own experience of treating infections in patients who receive immunosuppressant treatment. Results: Traditional immunomodulating treatment results in an increased risk of infection. The disease RA in itself increases the risk of infections. There is evidence of an increased incidence of infections with both extracellular bacteria and intracellular microorganisms such as mycobacteria, including Mycobacterium tuberculosis, and viruses in patients who are treated with TNF-ɑ inhibitors. Patients who are about to start taking TNF-ɑ inhibitors must therefore undergo a tuberculosis-risk assessment. Rituximab may increase the incidence of infection, but long-term observations are limited. Combination therapy involving different drugs that selectively modulate immune response is normally contraindicated because of the increased risk of infection. Interpretation: The benefit of TNF-ɑ inhibitors and rituximab treatment for RA must be weighed up against the increased risk of infections. Symptoms, findings and laboratory test results pertaining to serious infections may be influenced by immunomodulation therapy and thereby make clinical assessment difficult.
    Tidsskrift for den Norske laegeforening 09/2012; 132(16):1867-71. DOI:10.4045/tidsskr.12.0180
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    ABSTRACT: The purpose of this study was to investigate mediators of inflammation and haemostasis in patients with chronic necrotizing pulmonary aspergillosis (CNPA), a locally, destructive process of the lung due to invasion by Aspergillus species. Measurements of selected biomarkers in 10 patients with CNPA and 19 healthy, matched controls were performed with enzyme-linked immunosorbent assay (ELISA) and multiplex methodology. The gene expressions of relevant biomarkers were analyzed with real-time quantitative RT-PCR. Increased concentrations of circulating mediators of inflammation interleukin (IL)-6, IL-8, RANTES, TNF-α, ICAM-1 and mediators involved in endothelial activation and thrombosis (vWF, TF and PAI-1) were observed in patients with CNPA. The concentration of the anti-inflammatory cytokine IL-10 was increased both in plasma and in PBMC in the patient population. The gene expression of CD40L was decreased in PBMC from the patient group, accompanied by decreased concentrations of soluble (s) CD40L in the circulation. The proinflammatory response against Aspergillus may be counteracted by reduced CD40L and sCD40L, as well as increased IL-10, which may compromise the immune response against Aspergillus in patients with CNPA.
    BMC Infectious Diseases 06/2012; 12:144. DOI:10.1186/1471-2334-12-144 · 2.56 Impact Factor
    This article is viewable in ResearchGate's enriched format
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    ABSTRACT: Based on the ability to recruit lymphocytes and dendritic cells to lymphoid tissue and to promote inflammation, we hypothesized a role for dysregulated CCL19 and CCL21 levels in human immunodeficiency virus (HIV)-infected patients with advanced immunodeficiency, and in particular in those with accompanying Mycobacterium avium complex (MAC) infection. The hypothesis was explored by studies in HIV-infected patients with and without MAC infection, as well as in vitro, examining the ability of proteins from MAC to promote CCL19 and CCL21 responses in peripheral blood mononuclear cells (PBMC) during highly active anti-retroviral therapy (HAART). Our main findings were: (i) raised serum levels of CCL19 in HIV-infected patients with CD4(+) T cell count <50 cells/µl compared with HIV-infected patients with CD4(+) T cell count >500 cells/µl and healthy controls, with particularly high levels in those with MAC infection; (ii) elevated plasma levels of CCL19 predicted a higher mortality in acquired immune deficiency syndrome (AIDS)-patients, independent of ongoing MAC infection; and (iii) marked production of CCL19 in MAC-stimulated peripheral blood mononuclear cells (PBMC) and pronounced disturbances in MAC-induced CCL19 production in PBMC from HIV patients that was partly reversed during HAART. Our findings suggest the involvement of CCL19 in AIDS patients with advanced immunodeficiency, potentially mediating both adaptive and maladaptive responses.
    Clinical & Experimental Immunology 03/2012; 167(3):492-8. DOI:10.1111/j.1365-2249.2011.04524.x · 3.28 Impact Factor
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    Journal of Thrombosis and Haemostasis 02/2011; 9(5):1075-7. DOI:10.1111/j.1538-7836.2011.04242.x · 6.08 Impact Factor
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    ABSTRACT: Toll-like receptors (TLRs) are involved in the host defense against Aspergillus fumigatus infections, and some TLRs may even be exploited by the mould to escape immune mechanisms. We have previously shown that conidia from A. fumigatus increase expression of TLR5 in human monocytes. When further investigating a possible role of TLR5 in A. fumigatus infections, we observed a decrease in conidial viability after culturing with TLR5-knockdown THP-1 monocytes. Secondly, our experiments showed an increase in conidial viability when THP-1 monocytes, together with flagellin, are cultured with conidia. Thirdly, we found that treatment of THP-1 monocytes with a monoclonal antibody against TLR5 resulted in increased conidial viability after culturing. Experiments with a HEK-293 cell line only expressing TLR5 did not indicate that conidia directly interact with TLR5. Further studies of the intracellular molecular mechanisms activated concomitant with activation of TLR5 that have an enhancing effect on the viability of conidia may shed new light on the defense against conidia in monocytic cells, and possibly also on the function of the TLR5 system.
    Medical mycology: official publication of the International Society for Human and Animal Mycology 11/2010; 49(4):375-9. DOI:10.3109/13693786.2010.531772 · 2.26 Impact Factor
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    ABSTRACT: Patients with common variable immunodeficiency (CVID) have low serum IgG, IgA, and/or IgM levels and recurrent airway infections. Radiologic pulmonary abnormalities and impaired function are common complications. It is unclear to what extent IgG replacement treatment prevents further pulmonary damage and how factors beside infections may contribute to progression of disease. To study the development of pulmonary damage and determine how clinical and immunologic factors, such as serum IgG, may contribute to possible changes. In a retrospective, longitudinal study of 54 patients with CVID already treated with immunoglobulins, we examined changes of lung function and findings on high-resolution computed tomography (HRCT), obtained at 2 time points (the date of the last pulmonary function measurement before April 2005 [T1] and the date of the measurement performed closest to 5 years earlier [T0]) 2 to 7 years apart and explored possible relations to clinical and immunologic factors such as levels of IgG, tumor necrosis alpha (TNF-alpha), and mannose-binding lectin (MBL) in serum. Despite a mean (SD) serum IgG level of 7.6 (2.3) g/L for all the patients during the entire study period, lung function decreased from T0 to T1. The combination of a low serum IgA level and serum MBL was associated with the presence of bronchiectasis and lower lung function and with worsening of several HRCT abnormalities from T0 to T1. Increased serum levels of TNF-alpha were related to deterioration of gas diffusion. A mean serum IgG level less than 5 g/L between T0 and T1 was associated with worsening of linear and/or irregular opacities seen on HRCT. For a period of 4 years, lung function and HRCT deteriorated in CVID patients treated with immunoglobulins.
    Annals of allergy, asthma & immunology: official publication of the American College of Allergy, Asthma, & Immunology 06/2010; 104(6):503-10. DOI:10.1016/j.anai.2010.04.015 · 2.75 Impact Factor
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    JAIDS Journal of Acquired Immune Deficiency Syndromes 03/2010; 53(3):419-20. DOI:10.1097/QAI.0b013e3181ba4101 · 4.39 Impact Factor
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    Scandinavian Journal of Immunology 12/2009; 70(6):503-4. DOI:10.1111/j.1365-3083.2009.02343.x · 1.88 Impact Factor
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    ABSTRACT: Aspergillus fumigatus is the most frequent cause of invasive mold infections worldwide. Platelets contribute to inflammation and promote thrombosis, characteristically seen in aspergillosis, and might be involved both in antifungal defense and in the histopathological process. In the experiments reported here, in vitro activation of platelets by conidia, swollen conidia, and hyphae from A. fumigatus was assessed by flow cytometry and enzyme immunoassays. THP-1 monocytes and human monocytes with and without platelets were cultured with hyphae from A. fumigatus, and the release of interleukin-8 (IL-8) was measured by enzyme immunoassays. A. fumigatus potently induced the expression of CD62-p and CD63 and the release of CD40 ligand, RANTES, and Dickkopf homolog 1 in platelets, with particularly enhancing effects of hyphae compared with conidia. The hypha-mediated activation of platelets further enhanced the release of IL-8 both in THP-1 monocytes and in human adherent monocytes. In conclusion, we have found that A. fumigatus is a potent inducer of platelet-mediated inflammation, potentially promoting protective as well as harmful responses during aspergillosis.
    Infection and immunity 12/2009; 78(3):1269-75. DOI:10.1128/IAI.01091-09 · 4.16 Impact Factor
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    ABSTRACT: Activated platelets release a wide range of inflammatory mediators, including members of the tumour necrosis factor (TNF) superfamily (e.g. CD40 ligand [CD40L] and LIGHT). Such platelet-mediated inflammation could be involved in atherogenesis and plaque destabilisation. In the present study we investigated whether APRIL, another member of the TNF superfamily that has been detected in megakaryocytes, could be released from platelets upon activation. The release of APRIL was studied in thrombin receptor (SFLLRN) activated platelets, and the expression of APRIL was examined in plasma and within the atherosclerotic lesion in patients with carotid and coronary atherosclerosis. Upon SFLLRN activation, there was a gradual release of APRIL, reaching maximum after 90 minutes. While this pattern is similar to that of CD40L and LIGHT, the release of APRIL was quite differently regulated. Thus, prostaglandin E1, but not inhibitors of metal-dependent proteases and actin polymerisation or the lack of GP IIb/IIIa, blocks APRIL release in activated platelets. With relevance to atherogenesis, we found that patients with coronary artery disease (n=80) had raised plasma levels of APRIL as compared with controls (n=20), and APRIL immunoreactivity was detected in aggregated platelets within the ruptured plaque in patients with myocardial infarction and within macrophages in symptomatic carotid plaques. In conclusion, activated platelets release significant amounts of APRIL in a long-lasting manner, differently regulated than the gradual release of other platelet-derived TNF superfamily ligands. The enhanced expression of APRIL in atherosclerotic disorders, both systemically and within the lesion, may suggest a potential involvement of APRIL in atherogenesis.
    Thrombosis and Haemostasis 10/2009; 102(4):704-10. DOI:10.1160/TH08-10-0665 · 5.76 Impact Factor
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    ABSTRACT: CCL19 and CCL21 and their receptor CCR7 are expressed constitutively within lymphoid organs, regulating lymphocyte homing. Recent studies suggest that these chemokines may have inflammatory properties. We hypothesized a role of CCL19/CCL21 in human immunodeficiency virus (HIV) infection by promoting inflammation. We examined the expression of CCL19 and CCL21 in mononuclear cells from peripheral blood mononuclear cells (PBMC) and bone marrow mononuclear cells (BMMC) in HIV-infected patients before and during highly active anti-retroviral therapy (HAART). We also examined the ability of CCL19/CCL21 to promote inflammatory responses in these patients. PBMC from untreated HIV-infected patients (n = 29) released enhanced levels of CCL19 spontaneously compared with cells from controls (n = 20), particularly in those with symptomatic disease (n = 15, P < 0.01 versus controls). During HAART (n = 9), there was a decrease in the spontaneous CCL19 release and an increase in the phytohaemagglutinin-stimulated CCL19 release in both PBMC (P < 0.01) and BMMC (P < 0.05). In patients with enhanced HIV replication there was an increased proportion of inflammatory CD8(+)CCR7(-)CD45RA(-) T cells in peripheral blood [P < 0.01 and P < 0.05 versus controls, untreated (n = 9) and treatment failure (n = 8), respectively]. In vitro, CCL19/CCL21 promoted an inflammatory response in PBMC when accompanied by high viral load, irrespective of HAART. The HIV-tat protein significantly boosted the inflammatory effect of CCL19/CCL21 in PBMC. These findings link a dysregulated CCL19/CCL21/CCR7 system in HIV-infected patients to persistent inflammation and HIV replication, not only in untreated HIV infection, but also in treatment failure during HAART.
    Clinical & Experimental Immunology 09/2009; 157(3):400-7. DOI:10.1111/j.1365-2249.2009.03976.x · 3.28 Impact Factor
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    ABSTRACT: While some chemokines are thought to be protective in HIV-infected individuals by their ability to block HIV entry into T cells and macrophages, chemokines could also have harmful effects in HIV infection through their ability to promote inflammation. Here, we examined the regulation and the effects of CXCL16, a newly discovered chemokine of the CXC family, in HIV-infected patients. We examined serum levels of CXCL16 in clinically well-defined subgroups of HIV-infected individuals both before (n = 62) and during HAART (n = 40) as well as in age- and sex-matched healthy controls (n = 30). We also examined the effects of CXCL16 on inflammatory and anti-inflammatory cytokines and HIV replication in peripheral blood mononuclear cells (PBMC). Our main and novel findings were: (i) HIV-infected patients had significant raised CXCL16 levels according to disease severity and progression. (ii) During HAART, the immunological improvement was accompanied by a modest increase in CXCL16 level. (iii) While soluble CXCL16 promoted an anti-inflammatory response in PBMC from those on successful HAART, it induced an inflammatory response and enhanced HIV replication in PBMC from those with high viral load irrespectively of ongoing HAART. (iv) Recombinant HIV-tat protein significantly increased CXCL16 release in THP-1 macrophages. Our findings suggest a complex interaction between CXCL16 and HIV, promoting both inflammatory and anti-inflammatory effects as well as HIV replication, partly dependent on accompanying HIV replication.
    European Journal of Clinical Investigation 09/2009; 39(11):1017-24. DOI:10.1111/j.1365-2362.2009.02207.x · 3.37 Impact Factor
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    ABSTRACT: The ability to mount an oxidative burst (OB) in response to medium, zymosan and phorbol myristate acetate (PMA) was assessed in human blood monocytes cultured for 1 day (MO) and monocyte-derived macrophages cultured for 10 days (MDM). Further, the effect of recombinant interferons (IFNs) on OB generation was examined. The OB was measured as a reduction of nitroblue tetrazolium (NBT). Unstimulated and stimulated NBT reduction per cell nucleus and the ratio of stimulated/unstimulated NBT reduction was not significantly different in cells cultured for 1 and 10 days. In MO, IFN-γ stimulated the OB when co-stimulated with zymosan or PMA. IFN-α reduced MO adherence. When the lower adherence was corrected for, IFN-α enhanced NBT reduction. In MDM, a high concentration of IFN-γ stimulated the OB without co-stimulation, in lower concentrations the presence of a co-stimulant was necessary for OB stimulation. IFN-α/β enhanced the OB in response to PMA, suggesting that IFN-α/β has a role in macrophage activation.
    Apmis 08/2009; 97(1‐6):490 - 496. DOI:10.1111/j.1699-0463.1989.tb00821.x · 1.92 Impact Factor
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    ABSTRACT: Common variable immunodeficiency (CVID) is a heterogeneous syndrome characterized by defective immunoglobulin production and high frequency of bacterial infections, autoimmunity and manifestations of chronic inflammation. The homeostatic chemokines CCL19 and CCL21 and their receptor CCR7 are associated with modulation of inflammatory responses. CVID patients have decreased proportions of CCR7(+) T cells in peripheral blood and we hypothesized a further dysregulation of CCL19/CCL21/CCR7 in CVID. Serum levels of CCL19 and CCL21 were compared in CVID patients and controls. T cell expression of CCR7 was related to clinical characteristics in CVID patients. Spleens extirpated from CVID patients were analysed for expression of CCL19, CCL21 and CCR7. Peripheral blood mononuclear cells (PBMC) from CVID patients and controls were analysed for cytokine response on stimulation with CCL19 and CCL21. The main findings were: (i) CVID patients have raised serum levels of CCL19 and CCL21 independently of features of chronic inflammation; (ii) CCL19 and CCR7 have similar expression in spleens from CVID patients and controls, while CCL21 is variably down-regulated in spleens from patients; (iii) T cell expression of CCR7 is particularly low in patients characterized by chronic inflammation in vivo; and (iv) PBMC from CVID patients had attenuated cytokine response to stimulation with CCL19 and CCL21. CVID patients have raised circulatory levels of CCL19 and CCL21, and an attenuated cytokine response to stimulation with these chemokines. Because CCR7, CCL19 and CCL21 are key mediators balancing immunity and tolerance in the immune system, the abnormalities of these mediators might contribute to the profound immune dysregulation seen in CVID.
    Clinical & Experimental Immunology 08/2009; 158(2):237-45. DOI:10.1111/j.1365-2249.2009.04013.x · 3.28 Impact Factor
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    ABSTRACT: Among patients with recurrent, protracted or chronic infections of the respiratory tract involving the middle ear, 18 were found to have immunodeficiencies. In 10 of the patients, deficiency of immunoglobulins belonging to the IgG, IgA and IgM classes was found. Seven patients had an isolated IgA deficiency. One patient had a combined immunodeficiency with defects of the T-cell system and the B-cell system. One patient had an isolated T-cell deficiency.
    Acta Oto-Laryngologica 07/2009; 82(3-4):185-92. DOI:10.3109/00016487609120879 · 0.99 Impact Factor
  • American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California; 04/2009
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    ABSTRACT: Neutrophil gelatinase-associated lipocalin (NGAL or lipocalin-2) is a glycoprotein with bacteriostatic properties. Growing evidence suggests that NGAL may also be involved in cell survival, inflammation, and matrix degradation. We therefore aimed to investigate the role of NGAL in heart failure (HF). Our main findings were (i) patients with acute post-myocardial infarction (MI) HF (n = 236) and chronic HF (n = 150) had elevated serum levels of NGAL (determined by enzyme immunoassay), significantly correlated with clinical and neurohormonal deterioration, (ii) in patients with HF following acute MI, elevated NGAL levels of at baseline were associated with adverse outcomes (median of 27 months follow-up), (iii) in a rat model of post-MI HF, NGAL/lipocalin-2 gene expression was increased in the non-ischaemic part of the left ventricle primarily located to cardiomyocytes, (iv) strong NGAL immunostaining was found in cardiomyocytes within the failing myocardium both in experimental and clinical HF, (v) interleukin-1beta and agonists for toll-like receptors 2 and 4, representing components of the innate immune system, were potent inducers of NGAL/lipocalin-2 in isolated neonatal cardiomyocytes. Our demonstration of enhanced systemic and myocardial NGAL expression in clinical and experimental HF further support a role for innate immune responses in the pathogenesis of HF.
    European Heart Journal 04/2009; 30(10):1229-36. DOI:10.1093/eurheartj/ehp088 · 14.72 Impact Factor

Publication Stats

9k Citations
1,358.69 Total Impact Points


  • 1972–2013
    • Oslo University Hospital
      • Research Institute of Internal Medicine
      Kristiania (historical), Oslo County, Norway
    • Armauer Hansen Research Institute
      Ādīs Ābeba, Ādīs Ābeba, Ethiopia
  • 1973–2012
    • University of Oslo
      • • Research Institute for Internal Medicine (IIM)
      • • Department of Cardiology
      • • Division of Medicine
      • • Department of Paediatrics
      Kristiania (historical), Oslo County, Norway
  • 2009
    • St. Olavs Hospital
      Nidaros, Sør-Trøndelag, Norway
  • 2006
    • Karolinska University Hospital
      Tukholma, Stockholm, Sweden
  • 1998–2005
    • Diakonhjemmet Hospital (Norway)
      Kristiania (historical), Oslo, Norway
  • 2003
    • Haukeland University Hospital
      Bergen, Hordaland, Norway
    • Hospital Bærum
      Drammen, Buskerud county, Norway
  • 1976–2000
    • University of Bergen
      Bergen, Hordaland, Norway
    • The American University of Rome
      Roma, Latium, Italy
  • 1997–1999
    • Norwegian University of Science and Technology
      • Department of Cancer Research and Molecular Medicine
      Nidaros, Sør-Trøndelag, Norway
  • 1993
    • Institutt for samfunnsforskning, Oslo
      Kristiania (historical), Oslo County, Norway
  • 1976–1977
    • Karolinska Institutet
      • Department of Medicine, Huddinge
      Solna, Stockholm, Sweden