The use of ruminant ployclonal antibody (RPA) proteins for the prevention of allergic inflammation in the respiratoru tract

  • Rebecca Ford

    Research output: ThesisDoctoral Thesis

    279 Downloads (Pure)

    Abstract

    [Truncated abstract] Passive antibody immunotherapy, which utilises the great specificity and affinity of antibodies for pathogens or allergens, has become an area of increasing investigation for the prevention and treatment of human infectious and allergic diseases initiated at mucosal and other epithelial surfaces of the body. The respiratory tract has an extensive surface area in order to carry out the vital process of gaseous exchange between the atmosphere and internal body tissues. As a consequence, the resulting continuous environmental exposure inevitably renders this organ accessible to many pathological agents, chiefly infectious or allergic in origin. Thus, the primary stage of any respiratory inflammatory disease in response to external agents such as allergens involves contact between the agent and the delicate mucosal surfaces. This study investigated the hypothesis that passive treatment of the respiratory tract with heterologous antibodies of appropriate specificity, if present at the respiratory mucosal surface at the time of antigen exposure, could block mucosal binding of the antigen, thereby excluding it from contact with the host immune system (a process termed “immune exclusion”). An established ovalbumin (OVA) BALB/c mouse model of airways inflammation, in which sensitised mice develop airway inflammation in response to inhaled OVA challenge, was used to explore the potential for ruminant (ovine) polyclonal antibodies (RPAs) in mediating respiratory immune exclusion in the treatment and prevention of allergic airways inflammation.
    Original languageEnglish
    QualificationDoctor of Philosophy
    Publication statusUnpublished - 2012

    Fingerprint

    Dive into the research topics of 'The use of ruminant ployclonal antibody (RPA) proteins for the prevention of allergic inflammation in the respiratoru tract'. Together they form a unique fingerprint.

    Cite this