Marked induction of IL-6, haptoglobin and IFN gamma following experimental BRSV infection in young calves

Susanne Nedergaard Grell, Kirsten Tjørnehøj, Lars Erik Larsen, Peter M. H. Heegaard

    Research output: Contribution to journalJournal articleResearchpeer-review

    Abstract

    Bovine respiratory syncytial virus (BRSV) has been identified worldwide as an important pathogen associated with acute respiratory disease in calves. An infection model has been developed reflecting accurately the clinical course and die, development of pathological signs during a natural BRSV-infection. In the experiments described in the present study, calves were infected at 13-21 weeks of age and reinfected 14 weeks later. Blood samples front the entire infection period were analysed for acute phase protein (haptoglobin) by ELISA and for expression (mRNA level in peripheral blood mononuclear cells) of the cytokines interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6) and interferon-gamma (IFNgamma) by quantitative real-time reverse transcribed polymerase chain reaction (RT-PCR). IFNgamma, interleukin-6 and haptoglobin were markedly induced tot-ether with development of clinical signs in response to the first infection with BRSV The IFNgamma response was biphasic. with an early peak at day 1-3 post infection (p.i.) and a later increase between day 5 and 8 p.i. Reinfection also resulted in an induction of IFNgamma. but without induction of clinical signs, IL-6 and haptoglobin. These results indicate that early mediators connected with the innate responses are induced on a first encounter with the pathogen. but not on a second encounter (reinfection) where the adaptive immune system may act as the first line defence.
    Original languageEnglish
    JournalVeterinary Immunology and Immunopathology
    Volume103
    Issue number3-4
    Pages (from-to)235-245
    ISSN0165-2427
    DOIs
    Publication statusPublished - 2005

    Keywords

    • cytokines
    • bovine respiratory syncytial virus
    • acute phase proteins
    • experimental infection model

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