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Sökning: onr:"swepub:oai:lup.lub.lu.se:7fe5c82b-ab04-4043-b1fd-842ada332993" > A Murine Model for ...

  • Joma, Basma HTufts University School of Medicine (författare)

A Murine Model for Enhancement of Streptococcus pneumoniae Pathogenicity Upon Viral Infection and Advanced Age

  • Artikel/kapitelEngelska2021

Förlag, utgivningsår, omfång ...

  • 2021

Nummerbeteckningar

  • LIBRIS-ID:oai:lup.lub.lu.se:7fe5c82b-ab04-4043-b1fd-842ada332993
  • https://lup.lub.lu.se/record/7fe5c82b-ab04-4043-b1fd-842ada332993URI
  • https://doi.org/10.1128/IAI.00471-20DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

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

Anmärkningar

  • Streptococcus pneumoniae (pneumococcus) resides asymptomatically in the nasopharynx but can progress from benign colonizer to lethal pulmonary or systemic pathogen. Both viral infection and aging are risk factors for serious pneumococcal infections. Previous work established a murine model that featured the movement of pneumococcus from the nasopharynx to the lung upon nasopharyngeal inoculation with influenza A virus (IAV) but did not fully recapitulate the severe disease associated with human co-infection. We built upon this model by first establishing pneumococcal nasopharyngeal colonization, then inoculating both the nasopharynx and lungs with IAV. In young (2 months) mice, co-infection triggered bacterial dispersal from the nasopharynx into the lungs, pulmonary inflammation, disease and mortality in a fraction of mice. In old mice (20-22 months), co-infection resulted in earlier and more severe disease. Aging was not associated with greater bacterial burdens but rather with more rapid pulmonary inflammation and damage. Both aging and IAV infection led to inefficient bacterial killing by neutrophils ex vivo Conversely, aging and pneumococcal colonization also blunted IFN-α production and increased pulmonary IAV burden. Thus, in this multistep model, IAV promotes pneumococcal pathogenicity by modifying bacterial behavior in the nasopharynx, diminishing neutrophil function, and enhancing bacterial growth in the lung, while pneumococci increase IAV burden likely by compromising a key antiviral response. Thus, this model provides a means to elucidate factors, such as age and co-infection, that promote the evolution of S. pneumoniae from asymptomatic colonizer to invasive pathogen, as well as to investigate consequences of this transition on antiviral defense.

Ämnesord och genrebeteckningar

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

  • Siwapornchai, NalatTufts University School of Medicine (författare)
  • Vanguri, Vijay KUniversity of Massachusetts Medical School (författare)
  • Shrestha, AnishmaTufts University School of Medicine (författare)
  • Roggensack, Sara ETufts University School of Medicine (författare)
  • Davidson, Bruce AJacobs School of Medicine and Biomedical Sciences (författare)
  • Tai, Albert KTufts University School of Medicine (författare)
  • Hakansson, Anders PLund University,Lunds universitet,Institutionen för translationell medicin,Medicinska fakulteten,Experimentell infektionsmedicin, Malmö,Forskargrupper vid Lunds universitet,Department of Translational Medicine,Faculty of Medicine,Experimental Infection Medicine, Malmö,Lund University Research Groups(Swepub:lu)med-a1h (författare)
  • Meydani, Simin NJean Mayer USDA Human Nutrition Research Center on Aging (författare)
  • Leong, John MTufts University School of Medicine (författare)
  • Bou Ghanem, Elsa NJacobs School of Medicine and Biomedical Sciences (författare)
  • Tufts University School of MedicineUniversity of Massachusetts Medical School (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Infection and Immunity89:81098-5522

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