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Polymeric Ig recept...
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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 ...
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2006-03-28
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Oxford university press,2006
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:su-23601
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https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-23601URI
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https://doi.org/10.1093/intimm/dxl017DOI
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https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-23926URI
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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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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Rodríguez, ArianeStockholms universitet,Wenner-Grens institut
(author)
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Cardona, P J
(author)
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Guirado, E
(author)
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Ivanyi, J
(author)
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Singh, M
(author)
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Marsh, P.D.
(author)
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Williams, A
(author)
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Troye-Blomberg, MaritaStockholms universitet,Avdelningen för immunologi(Swepub:su)marita
(author)
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Fernandez, Carmen
(author)
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Stockholms universitetAvdelningen för immunologi
(creator_code:org_t)
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In:International Immunology: Oxford university press18:5, s. 807-8160953-81781460-2377
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Tjärnlund, Anna
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Rodríguez, Arian ...
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Cardona, P J
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Guirado, E
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Ivanyi, J
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Singh, M
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Marsh, P.D.
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Williams, A
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Troye-Blomberg, ...
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Fernandez, Carme ...
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and Immunology
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Stockholm University