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Cutting edge: guinea pigs with a natural C3a-receptor defect exhibit decreased bronchoconstriction in allergic airway disease: evidence for an involvement of the C3a anaphylatoxin in the pathogenesis of asthma.

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Affiliations

  • 1. Institute of Medical Microbiology, Medical School, Hannover, Germany.
      Authors
    • Bautsch W 1
    (1 author)

Journal of Immunology (Baltimore, Md. : 1950), 01 Nov 2000, 165(10):5401-5405
https://doi.org/10.4049/jimmunol.165.10.5401 PMID: 11067890 

Abstract 

Asthma is a major cause of morbidity worldwide with prevalence and severity still increasing at an alarming pace. Hallmarks of this disease include early-phase bronchoconstriction with subsequent eosinophil infiltration, symptoms that may be mimicked in vivo by the complement-derived C3a anaphylatoxin, following its interaction with the single-copy C3aR. We analyzed the pathophysiological role of the C3a anaphylatoxin in a model of experimental OVA-induced allergic asthma, using an inbred guinea pig strain phenotypically unresponsive to C3a. Molecular analysis of this defect revealed a point mutation within the coding region of the C3aR that creates a stop codon, thereby effectively inactivating gene function. When challenged by OVA inhalation, sensitized animals of this strain exhibited a bronchoconstriction decreased by approximately 30% in comparison to the corresponding wild-type strain. These data suggest an important role of C3a in the pathogenesis of asthma and define a novel target for drug intervention strategies.

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Read article at publisher's site: https://doi.org/10.4049/jimmunol.165.10.5401

Read article for free, from open access legal sources, via Unpaywall: https://www.jimmunol.org/content/jimmunol/165/10/5401.full.pdfUnpaywall

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