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  • Alizadehgharib, SaraGothenburg University,Göteborgs universitet,Institutionen för odontologi, sektion 3,Institute of Odontology, Section 3 (författare)

Immunological response of human leucocytes after exposure to lipopolysaccharides from Porphyromonas gingivalis.

  • Artikel/kapitelEngelska2021

Förlag, utgivningsår, omfång ...

  • 2020-12-29
  • Wiley,2021

Nummerbeteckningar

  • LIBRIS-ID:oai:gup.ub.gu.se/300547
  • https://gup.ub.gu.se/publication/300547URI
  • https://doi.org/10.1002/cre2.388DOI

Kompletterande språkuppgifter

  • Språk:engelska

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Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Porphyromonas gingivalis (P. gingivalis) is a gram-negative bacterium and an important etiologic agent of periodontitis. P. gingivalis releases outer membrane vesicles containing lipopolysaccharides (LPS), which can penetrate periodontal tissues. Once in the periodontal tissues and in contact with immune cells, it may participate in the destructive innate host response associated with the disease. The exact mechanism of P. gingivalis LPS in the disease process is not clear, but it is known to affect a variety of immune responses.To investigate how LPS from P. gingivalis affect neutrophil extracellular trap (NET) formation, cell death and production of cytokines from human neutrophils and peripheral mononuclear blood mononuclear cells (PBMCs).Isolated neutrophils and PBMCs were cultured with LPS from P. gingivalis or Escherichia coli (E. coli) (control). The NET formation was measured using Sytox green stain. Cell death of neutrophils and PBMCs was analyzed using flow cytometry or Sytox green stain. Cytokine production was measured using enzyme-linked immunosorbent assay (ELISA) kit or Bio-Plex assay.Exposure to LPS from P. gingivalis and E. coli caused significantly lower cell death in neutrophils. NETs were formed after exposure to the two different LPS. In PBMCs, exposure to P. gingivalis and E. coli LPS caused increased levels of IL-1β and IL-6 compared to unstimulated controls. Increased cell death in PBMCs after exposure to LPS from E. coli in comparison to LPS from P. gingivalis and unstimulated controls was also observed.LPS from P. gingivalis has the ability to affect both human neutrophils and PBMCs with regard to cytokine production, cell death and production of NETs. LPS from P. gingivalis could be involved in the pathogenesis of periodontitis, and our results may contribute information regarding possible markers for diagnosis and targets for treatment of periodontal disease.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Östberg, Anna-karin,1979Gothenburg University,Göteborgs universitet,Institutionen för odontologi, sektion 3,Institute of Odontology, Section 3(Swepub:gu)xoannr (författare)
  • Dahlstrand Rudin, AgnesGothenburg University,Göteborgs universitet,Institutionen för odontologi, sektion 3,Institute of Odontology, Section 3(Swepub:gu)xdahis (författare)
  • Dahlgren, Ulf,1953Gothenburg University,Göteborgs universitet,Institutionen för odontologi, sektion 3,Institute of Odontology, Section 3(Swepub:gu)xdahlu (författare)
  • Christenson, KarinGothenburg University,Göteborgs universitet,Institutionen för odontologi, sektion 3,Institute of Odontology, Section 3(Swepub:gu)xchrka (författare)
  • Göteborgs universitetInstitutionen för odontologi, sektion 3 (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Clinical and experimental dental research: Wiley7:4, s. 531-5382057-4347

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