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Search: WFRF:(Rees Sophie) > (2020-2024)

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1.
  • Kommula, S. M., et al. (author)
  • Effect of Long-Range Transported Fire Aerosols on Cloud Condensation Nuclei Concentrations and Cloud Properties at High Latitudes
  • 2024
  • In: Geophysical Research Letters. - 0094-8276 .- 1944-8007. ; 51:6
  • Journal article (peer-reviewed)abstract
    • Active vegetation fires in south-eastern (SE) Europe resulted in a notable increase in the number concentration of aerosols and cloud condensation nuclei (CCN) particles at two high latitude locations—the SMEAR IV station in Kuopio, Finland, and the Zeppelin Observatory in Svalbard, high Arctic. During the fire episode aerosol hygroscopicity κ slightly increased at SMEAR IV and at the Zeppelin Observatory κ decreased. Despite increased κ in high CCN conditions at SMEAR IV, the aerosol activation diameter increased due to the decreased supersaturation with an increase in aerosol loading. In addition, at SMEAR IV during the fire episode, in situ measured cloud droplet number concentration (CDNC) increased by a factor of ∼7 as compared to non-fire periods which was in good agreement with the satellite observations (MODIS, Terra). Results from this study show the importance of SE European fires for cloud properties and radiative forcing in high latitudes.
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2.
  • Strickson, Sam, et al. (author)
  • Oxidised IL-33 drives COPD epithelial pathogenesis via ST2-independent RAGE/EGFR signalling complex
  • 2023
  • In: European Respiratory Journal. - 0903-1936. ; 62:3
  • Journal article (peer-reviewed)abstract
    • Background Epithelial damage, repair and remodelling are critical features of chronic airway diseases including chronic obstructive pulmonary disease (COPD). Interleukin (IL)-33 released from damaged airway epithelia causes inflammation via its receptor, serum stimulation-2 (ST2). Oxidation of IL-33 to a non-ST2-binding form (IL-33ox) is thought to limit its activity. We investigated whether IL-33ox has functional activities that are independent of ST2 in the airway epithelium. Methods In vitro epithelial damage assays and three-dimensional, air–liquid interface (ALI) cell culture models of healthy and COPD epithelia were used to elucidate the functional role of IL-33ox. Transcriptomic changes occurring in healthy ALI cultures treated with IL-33ox and COPD ALI cultures treated with an IL-33-neutralising antibody were assessed with bulk and single-cell RNA sequencing analysis. Results We demonstrate that IL-33ox forms a complex with receptor for advanced glycation end products (RAGE) and epidermal growth factor receptor (EGFR) expressed on airway epithelium. Activation of this alternative, ST2-independent pathway impaired epithelial wound closure and induced airway epithelial remodelling in vitro. IL-33ox increased the proportion of mucus-producing cells and reduced epithelial defence functions, mimicking pathogenic traits of COPD. Neutralisation of the IL-33ox pathway reversed these deleterious traits in COPD epithelia. Gene signatures defining the pathogenic effects of IL-33ox were enriched in airway epithelia from patients with severe COPD. Conclusions Our study reveals for the first time that IL-33, RAGE and EGFR act together in an ST2-independent pathway in the airway epithelium and govern abnormal epithelial remodelling and mucoobstructive features in COPD.
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