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  • 1.
    Nielsen, Jens
    KTH, Centres, Science for Life Laboratory, SciLifeLab. Chalmers University of Technology, Sweden.
    Metabolism: Built on stable catalysts2017In: Nature Microbiology, E-ISSN 2058-5276, Vol. 2, no 7, article id 17085Article in journal (Refereed)
  • 2.
    Subramanian, Karthik
    et al.
    Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden..
    Neill, Daniel R.
    Univ Liverpool, Inst Infect & Global Hlth, Liverpool, Merseyside, England..
    Malak, Hesham A.
    Univ Liverpool, Inst Infect & Global Hlth, Liverpool, Merseyside, England..
    Spelmink, Laura
    Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden..
    Khandaker, Shadia
    Univ Liverpool, Inst Infect & Global Hlth, Liverpool, Merseyside, England..
    Marchiori, Giorgia Dalla Libera
    Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden..
    Dearing, Emma
    Univ Liverpool, Inst Infect & Global Hlth, Liverpool, Merseyside, England..
    Kirby, Alun
    Univ York, Ctr Immunol & Infect, Dept Biol, York, N Yorkshire, England.;Univ York, Hull York Med Sch, York, N Yorkshire, England..
    Yang, Marie
    Univ Liverpool, Inst Infect & Global Hlth, Liverpool, Merseyside, England..
    Achour, Adnane
    Karolinska Inst, Dept Med Solna, Sci Life Lab, Stockholm, Sweden.;Karolinska Univ Hosp Solna, Dept Infect Dis, Stockholm, Sweden..
    Nilvebrant, Johan
    KTH, School of Engineering Sciences in Chemistry, Biotechnology and Health (CBH), Protein Science, Protein Technology.
    Nygren, Per-Åke
    KTH, School of Engineering Sciences in Chemistry, Biotechnology and Health (CBH), Protein Science, Protein Technology.
    Plant, Laura
    Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden..
    Kadioglu, Aras
    Univ Liverpool, Inst Infect & Global Hlth, Liverpool, Merseyside, England..
    Henriques-Normark, Birgitta
    Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden.;Karolinska Univ Hosp Solna, Clin Microbiol, Stockholm, Sweden.;Nanyang Technol Univ, Lee Kong Chian Sch Med LKC, Singapore, Singapore.;Nanyang Technol Univ, SCELSE, Singapore, Singapore..
    Pneumolysin binds to the mannose receptor C type 1 (MRC-1) leading to anti-inflammatory responses and enhanced pneumococcal survival2019In: Nature Microbiology, E-ISSN 2058-5276, Vol. 4, no 1, p. 62-70Article in journal (Refereed)
    Abstract [en]

    Streptococcus pneumoniae (the pneumococcus) is a major cause of mortality and morbidity globally, and the leading cause of death in children under 5 years old. The pneumococcal cytolysin pneumolysin (PLY) is a major virulence determinant known to induce pore-dependent pro-inflammatory responses. These inflammatory responses are driven by PLY-host cell membrane cholesterol interactions, but binding to a host cell receptor has not been previously demonstrated. Here, we discovered a receptor for PLY, whereby pro-inflammatory cytokine responses and Toll-like receptor signalling are inhibited following PLY binding to the mannose receptor C type 1 (MRC-1) in human dendritic cells and mouse alveolar macrophages. The cytokine suppressor SOCS1 is also upregulated. Moreover, PLY-MRC-1 interactions mediate pneumococcal internalization into non-lysosomal compartments and polarize naive T cells into an interferon-gamma(low), interleukin-4(high) and FoxP3(+) immunoregulatory phenotype. In mice, PLY-expressing pneumococci colocalize with MRC-1 in alveolar macrophages, induce lower pro-inflammatory cytokine responses and reduce neutrophil infiltration compared with a PLY mutant. In vivo, reduced bacterial loads occur in the airways of MRC-1-deficient mice and in mice in which MRC-1 is inhibited using blocking antibodies. In conclusion, we show that pneumococci use PLY-MRC-1 interactions to downregulate inflammation and enhance bacterial survival in the airways. These findings have important implications for future vaccine design.

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