| 1. |
- Eggers, Jeannette, et al.
(author)
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Balancing wood production and biodiversity in intensively managed boreal forest
- 2022
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In: Scandinavian Journal of Forest Research. - : Informa UK Limited. - 0282-7581 .- 1651-1891.
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Journal article (peer-reviewed)abstract
- Fennoscandian boreal forests are managed intensively for wood production, which has had a negative impact on biodiversity. The harvesting pressure on the forests is likely to increase in the future because wood is seen as an important resource in a bio-based economy. Thus, there is an urgent need to better describe the trade-offs between wood production and biodiversity, and to understand how these trade-offs can be alleviated by adapting forest management. Encompassing a broad range of biodiversity aspects, we studied how forest management can increase biodiversity indicators while maintaining or increasing current harvest levels. We found that there is considerable leeway for forestry to pursue multiple objectives simultaneously in Fennoscandian forest landscapes. We show that it is possible to both increase harvests and structural elements of importance for biodiversity compared to present levels in a forest landscape that is representative of conditions in boreal forests in northern Sweden. Achieving this requires a variation in management strategies at the landscape level, and an adaptation of management practices to explicitly consider and implement multiple objectives in the planning process.
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| 2. |
- Johansson, Linda, et al.
(author)
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HMGB1 in severe soft tissue infections caused by Streptococcus pyogenes.
- 2014
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In: Frontiers in cellular and infection microbiology. - : Frontiers Media SA. - 2235-2988. ; 4:Jan 30
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Journal article (peer-reviewed)abstract
- Extracellular High Mobility Group Box 1 (HMGB1) has been associated with acute and chronic inflammatory conditions. However, little is known about HMGB1 in necrotizing bacterial infections. We hypothesized that the local HMGB1 response is excessive in severe soft tissue infections (STIs), which are characterized by necrosis and hyperinflammation. To explore this, tissue biopsies were collected from patients with varying severity of Streptococcus pyogenes skin and STIs, including erysipelas, cellulitis, and necrotizing fasciitis. Tissue sections were immunostained for HMGB1, S. pyogenes, and inflammatory cell infiltrates and results quantified by acquired computerized image analysis (ACIA). HMGB1 expression increased in parallel to disease severity and was significantly higher in necrotizing fasciitis than in erysipelas (p = 0.0023). Confocal microscopy of sections co-stained for HMGB1 and cell markers revealed both extracellular and cytoplasmic HMGB1, the latter of which was found predominantly in macrophages. To further verify macrophages as main source of activation triggered HMGB1 release, human macrophages were infected with clinical S. pyogenes isolates. The results demonstrated infection triggered release of HMGB1. Dual staining's visualized HMGB1 in areas close to, but not overlapping, with neutrophils, indicating a potential chemotactic role. In vitro transmigration experiments showed a chemotactic effect of HMGB1 on neutrophils. The data furthermore provided in vivo support that HGMB1 may form immunostimulatory complexes with IL-1β. Taken together, the findings provide the first in vivo evidence that HMGB1 is abundant at the local site of severe bacterial STIs and its levels correlated to severity of infections; hence, indicating its potential value as a biomarker for tissue pathology.
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| 3. |
- Klein, Julian, et al.
(author)
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Climate targets in European timber-producing countries conflict with goals on forest ecosystem services and biodiversity
- 2023
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In: Communications earth & environment. - 2662-4435. ; 4
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Journal article (peer-reviewed)abstract
- The role of increased timber harvests in reaching climate mitigation targets for European countries will be limited if the protection of forest ecosystem services and biodiversity is to be achieved, suggests an empirical forest model driven by future scenarios to limit warming to 1.5 degrees C in 2100.The European Union (EU) set clear climate change mitigation targets to reach climate neutrality, accounting for forests and their woody biomass resources. We investigated the consequences of increased harvest demands resulting from EU climate targets. We analysed the impacts on national policy objectives for forest ecosystem services and biodiversity through empirical forest simulation and multi-objective optimization methods. We show that key European timber-producing countries - Finland, Sweden, Germany (Bavaria) - cannot fulfil the increased harvest demands linked to the ambitious 1.5 degrees C target. Potentials for harvest increase only exists in the studied region Norway. However, focusing on EU climate targets conflicts with several national policies and causes adverse effects on multiple ecosystem services and biodiversity. We argue that the role of forests and their timber resources in achieving climate targets and societal decarbonization should not be overstated. Our study provides insight for other European countries challenged by conflicting policies and supports policymakers.
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| 4. |
- Mazziotta, Adriano, et al.
(author)
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More future synergies and less trade-offs between forest ecosystem services with natural climate solutions instead of bioeconomy solutions
- 2022
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In: Global Change Biology. - : Wiley. - 1354-1013 .- 1365-2486. ; 28, s. 6333-6348
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Journal article (peer-reviewed)abstract
- To reach the Paris Agreement, societies need to increase the global terrestrial carbon sink. There are many climate change mitigation solutions (CCMS) for forests, including increasing bioenergy, bioeconomy, and protection. Bioenergy and bioeconomy solutions use climate-smart, intensive management to generate high quantities of bioenergy and bioproducts. Protection of (semi-)natural forests is a major component of "natural climate solution" (NCS) since forests store carbon in standing biomass and soil. Furthermore, protected forests provide more habitat for biodiversity and non-wood ecosystem services (ES). We investigated the impacts of different CCMS and climate scenarios, jointly or in isolation, on future wood ES, non-wood ES, and regulating ES for a major wood provider for the international market. Specifically, we projected future ES given by three CCMS scenarios for Sweden 2020-2100. In the long term, fulfilling the increasing wood demand through bioenergy and bioeconomy solutions will decrease ES multifunctionality, but the increased stand age and wood stocks induced by rising greenhouse gas (GHG) concentrations will partially offset these negative effects. Adopting bioenergy and bioeconomy solutions will have a greater negative impact on ES supply than adopting NCS. Bioenergy or bioeconomy solutions, as well as increasing GHG emissions, will reduce synergies and increase trade-offs in ES. NCS, by contrast, increases the supply of multiple ES in synergy, even transforming current ES trade-offs into future synergies. Moreover, NCS can be considered an adaptation measure to offset negative climate change effects on the future supplies of non-wood ES. In boreal countries around the world, forestry strategies that integrate NCS more deeply are crucial to ensure a synergistic supply of multiple ES.
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| 5. |
- Neumann, Ariane, et al.
(author)
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Immunoregulation of Neutrophil Extracellular Trap Formation by Endothelial-Derived p33 (gC1q Receptor)
- 2018
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In: Journal of Innate Immunity. - : S. Karger AG. - 1662-811X .- 1662-8128. ; 10:1, s. 30-43
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Journal article (peer-reviewed)abstract
- The formation of neutrophil extracellular traps (NETs) is a host defence mechanism, known to facilitate the entrapment and growth inhibition of many bacterial pathogens. It has been implicated that the translocation of myeloperoxidase (MPO) from neutrophilic granules to the nucleus is crucial to this process. Under disease conditions, however, excessive NET formation can trigger self-destructive complications by releasing pathologic levels of danger-associated molecular pattern molecules (DAMPs). To counteract such devastating immune reactions, the host has to rely on precautions that help circumvent these deleterious effects. Though the induction of DAMP responses has been intensively studied, the mechanisms that are used by the host to down-regulate them are still not understood. In this study, we show that p33 is an endothelial-derived protein that has the ability to annul NET formation. We found that the expression of human p33 is up-regulated in endothelial cells upon infections with Streptococcus pyogenes bacteria. Using tissue biopsies from a patient with streptococcal necrotising fasciitis, we monitored co-localisation of p33 with MPO. Further in vitro studies revealed that p33 is able to block the formation of DAMP-induced NET formation by inhibiting the enzymatic activity of MPO. Additionally, mice challenged with S. pyogenes bacteria demonstrated diminished MPO activity when treated with p33. Together, our results demonstrate that host-derived p33 has an important immunomodulating function that helps to counterbalance an overwhelming DAMP response.
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| 6. |
- Snäll, Johanna, et al.
(author)
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Differential neutrophil responses to bacterial stimuli: Streptococcal strains are potent inducers of heparin-binding protein and resistin-release.
- 2016
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In: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 6
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Journal article (peer-reviewed)abstract
- Neutrophils are critical for the control of bacterial infections, but they may also contribute to disease pathology. Here we explore neutrophil responses, in particular the release of sepsis-associated factors heparin-binding protein (HBP) and resistin in relation to specific bacterial stimuli and sepsis of varying aetiology. Analyses of HBP and resistin in plasma of septic patients revealed elevated levels as compared to non-infected critically ill patients. HBP and resistin correlated significantly in septic patients, with the strongest association seen in group A streptococcal (GAS) cases. In vitro stimulation of human neutrophils revealed that fixed streptococcal strains induced significantly higher release of HBP and resistin, as compared to Staphylococcus aureus or Escherichia coli. Similarly, neutrophils stimulated with the streptococcal M1-protein showed a significant increase in co-localization of HBP and resistin positive granules as well as exocytosis of these factors, as compared to LPS. Using a GAS strain deficient in M1-protein expression had negligible effect on neutrophil activation, while a strain deficient in the stand-alone regulator MsmR was significantly less stimulatory as compared to its wild type strain. Taken together, the findings suggest that the streptococcal activation of neutrophils is multifactorial and involves, but is not limited to, proteins encoded by the FCT-locus.
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| 7. |
- Snäll, Johanna
(author)
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Phagocytic cells and Streptococcus pyogenes in invasive infections : an inflammatory relationship
- 2017
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Doctoral thesis (other academic/artistic)abstract
- Severe Streptococcus pyogenes infections, such as streptococcal toxic shock syndrome and necrotizing soft tissue infections, are rare but life threatening conditions. They are characterized by high bacterial load and a hyper-inflammatory state. The aim of this thesis was to investigate interactions between S. pyogenes and the phagocytic cells neutrophils and macrophages and how this correlates to cell activation and inflammation. First, we investigated high mobility group box 1 (HMGB1), a marker of inflammation and necrosis, as a potential biomarker and mediator of tissue pathology in S. pyogenes tissue infections. Analysis of tissue biopsies collected from patients with streptococcal soft tissue infections of varying severity showed that HMGB1 was present in the tissue, and that the amount correlates with severity. Further investigations showed that HMGB1 co-localized with IL-1β suggesting the potential for immunostimulatory complexes to form at the site of infection. HMGB1 was also demonstrated to act as a chemoattractant for neutrophils. Next, we assessed neutrophil activation and degranulation in response to different bacterial species, focusing on the release of the sepsis-associated factors heparin-binding protein (HBP) and resistin. Stimulations of neutrophils showed that streptococcal strains were potent inducers of neutrophil activation and degranulation. The results also showed a difference in signaling requirements for the release of HBP and resistin, respectively. While HBP release was mainly dependent on a previously described mechanism involving dual ligation of integrins and Fc-receptors, the release of resistin appeared to be multifactorial and involve multiple bacterial structures and host signaling pathways. Finally, we set out to define the macrophage phenotype present at the site of infection. Using a multi-parameter imaging workflow, we were able to assess the phenotype of macrophages present at the site of infection, in tissue from patients with severe S. pyogenes soft tissue infections as well as infected organotypic skin tissue models. These investigations showed that macrophages in S. pyogenes infected tissue displayed a shift towards a more anti- inflammatory M2-like phenotype, in spite of the hyper-inflammatory environment in the tissue. Gene expression analysis of infected patient tissue, skin tissue models as well as a murine model of severe streptococcal soft tissue infection showed an overrepresentation of signaling pathways associated with anti-inflammatory macrophage polarization. Taken together these findings highlight the complex pathophysiology of severe S. pyogenes infections, where on the one hand the bacteria and mediators present in the infected tissue potently activates neutrophils. While macrophages on the other hand, display a more anti- inflammatory phenotype upon infection, potentially promoting intracellular survival and persistence of S. pyogenes. Emphasizing the importance of careful patient characterization with regards to immune status, to ensure optimal treatment.
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| 8. |
- Thomsson, Elisabeth, 1975, et al.
(author)
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Recombinant glycoprotein E produced in mammalian cells in large-scale as an antigen for varicella-zoster-virus serology.
- 2011
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In: Journal of virological methods. - : Elsevier BV. - 1879-0984 .- 0166-0934. ; 175:1, s. 53-9
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Journal article (peer-reviewed)abstract
- A recombinant glycoprotein E (gE) from varicella-zoster virus (VZV) was generated and produced in Chinese Hamster Ovary (CHO) cells, in the development of a specific antigen for analysis of IgG antibodies to VZV. Several stable gE-secreting clones were established and one clone was adapted to growth in serum-free suspension culture. When the cells were cultured in a perfusion bioreactor, gE was secreted into the medium, from where it could be easily purified. The recombinant gE was then evaluated as a serological antigen in ELISA. When compared to a conventional whole virus antigen, the VZV gE showed similar results in ELISA-based seroprevalence studies of 854 samples derived from blood donors, students, ischemic stroke patients and their controls, including samples with border-line results in previous analyses. Eight samples (0.9%) were discordant, all being IgG-negative by the VZV gE ELISA and positive by the whole virus ELISA. The sensitivity and specificity of the VZV gE ELISA were 99.9% and 100%, respectively, compared to 100% and 88.9% for the VZV whole virus ELISA. The elderly subjects showed similar reactivities to both antigens, while VZV gE gave lower signals in the younger cohorts, suggesting that antibodies to gE may increase with age. It was concluded that the recombinant VZV gE from CHO cells was suitable as a serological antigen for the detection of IgG antibodies specific for VZV.
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| 9. |
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| 10. |
- Westman, Johannes, et al.
(author)
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Protein SIC secreted from Streptococcus pyogenes forms complexes with extracellular histones that boost cytokine production
- 2018
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In: Frontiers in Immunology. - : Frontiers Media SA. - 1664-3224. ; 9:FEB, s. 1-14
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Journal article (peer-reviewed)abstract
- Innate immunity relies on an effective recognition of the pathogenic microorganism as well as on endogenous danger signals. While bacteria in concert with their secreted virulence factors can cause a number of inflammatory reactions, danger signals released at the site of infection may in addition determine the amplitude of such responses and influence the outcome of the disease. Here, we report that protein SIC, Streptococcal Inhibitor of Complement, an abundant secreted protein from Streptococcus pyogenes, binds to extracellular histones, a group of danger signals released during necrotizing tissue damage. This interaction leads to the formation of large aggregates in vitro. Extracellular histones and SIC are abundantly expressed and seen colocalized in biopsies from patients with necrotizing soft-tissue infections caused by S. pyogenes. In addition, binding of SIC to histones neutralized their antimicrobial activity. Likewise, the ability of histones to induce hemolysis was inhibited in the presence of SIC. However, when added to whole blood, SIC was not able to block the pro-inflammatory effect of histones. Instead SIC boosted the histone-triggered release of a broad range of cytokines and chemokines, including IL-6, TNF-α, IL-8, IL-1β, IL-1ra, G-CSF, and IFN-γ. These results demonstrate that the interaction between SIC and histones has multiple effects on the host response to S. pyogenes infection.
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