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  • Tjärnlund, AnnaStockholms universitet,Avdelningen för immunologi,Wenner-Grens institut (author)

Polymeric Ig receptor knockout mice are more susceptible to mycobacteria infection in the respiratory tract

  • Article/chapterEnglish2006

Publisher, publication year, extent ...

  • 2006-03-28
  • Oxford university press,2006
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:su-23601
  • https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-23601URI
  • https://doi.org/10.1093/intimm/dxl017DOI
  • https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-23926URI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • It is generally accepted that cellular, and not humoral immunity, plays the crucial role in defense against intracellular bacteria. However, accumulating data indicate the importance of humoral immunity for the defense against a number of intracellular bacteria, including mycobacteria. We have investigated the role of secretory IgA, the main isotype found in mucosal tissues, in protection against mycobacterial infection, using polymeric IgR (pIgR)-deficient mice. Characterization of the humoral response induced after intra-nasal immunizations with the mycobacterial antigen PstS-1 revealed a loss of antigen-specific IgA response in saliva from the knockout mice. IgA level in the bronchoalveolar lavage of knockout mice was similar to wild-type level, although the IgA antibodies must have reached the lumen by other means than pIgR-mediated transport. Infection with Mycobacterium bovis bacillus Calmette–Guérin (BCG) demonstrated that the immunized pIgR−/− mice were more susceptible to BCG infection than immunized wild-type mice, based on higher bacterial loads in the lungs. This was accompanied by a reduced production of both IFN-γ and tumor necrosis factor-alpha (TNF-α) in the lungs. Additionally, the pIgR−/− mice displayed reduced natural resistance to mycobacterial infection proved by significantly higher bacterial growth in their lungs compared with wild-type mice after infection with virulent Mycobacterium tuberculosis. The knockout mice appeared to have a delayed mycobacteria-induced immune response with reduced expression of protective mediators, such as IFN-γ, TNF-α, inducible nitric oxide synthase and regulated upon activation normal T cell sequence, during early infection. Collectively, our results show that actively secreted IgA plays a role in protection against mycobacterial infections in the respiratory tract, by blocking entrance of bacilli into the lungs, in addition to modulation of the mycobacteria-induced pro-inflammatory response.

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Added entries (persons, corporate bodies, meetings, titles ...)

  • Rodríguez, ArianeStockholms universitet,Wenner-Grens institut (author)
  • Cardona, P J (author)
  • Guirado, E (author)
  • Ivanyi, J (author)
  • Singh, M (author)
  • Marsh, P.D. (author)
  • Williams, A (author)
  • Troye-Blomberg, MaritaStockholms universitet,Avdelningen för immunologi(Swepub:su)marita (author)
  • Fernandez, Carmen (author)
  • Stockholms universitetAvdelningen för immunologi (creator_code:org_t)

Related titles

  • In:International Immunology: Oxford university press18:5, s. 807-8160953-81781460-2377

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