Ennis, D.P., Cassidy, Joseph P. and Mahon, Bernard P. (2004) Prior Bordetella pertussis infection modulates allergen priming and the severity of airway pathology in a murine model of allergic asthma. Clinical and Experimental Allergy, 34. pp. 1488-1497.
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Abstract
Background It has been proposed that T helper (Th)2-driven immune deviation in early life can be
countered by Th1 inducing childhood infections and that such counter-regulation can protect against
allergic asthma.
Objective To test whether Th1-inducing infection with Bordetella pertussis protects against allergic
asthma using well-characterized murine models.
Methods Groups of mice were sensitized to ovalbumin (OVA) in the presence or absence of
B. pertussis, a well-characterized Th1 inducing respiratory infection. Immunological, pathological
and physiological parameters were measured to assess the impact of infection on immune deviation
and airway function.
Results We demonstrate that OVA sensitization does not affect the development of B. pertussisspecific
immune responses dominated by IgG2a and IFN-g and does not impair Th1-mediated
clearance of airway infection. In contrast, B. pertussis infection at the time of sensitization modulated
the response to OVA and significantly reduced total serum and OVA-specific IgE. The pattern of
cytokine responses, in particular OVA-specific IL-5 responses in the spleen was also modulated.
However, B. pertussis did not cause global suppression as IL-10 and IL-13 levels were enhanced in
OVA-stimulated spleen cell cultures and in lavage fluid from infected co-sensitized mice.
Histopathological examination revealed that B. pertussis infection prior to OVA sensitization
resulted in increased inflammation of bronchiolar walls with accompanying hyperplasia and mucous
metaplasia of lining epithelia. These pathological changes were accompanied by increased bronchial
hyper-reactivity to methacholine exposure.
Conclusion Contrary to the above premise, a Th1 response induced by a common childhood
infection does not protect against bronchial hyper-reactivity, but rather exacerbates the allergic
asthmatic response, despite modulation of immune mediators.
Item Type: | Article |
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Keywords: | allergy, bacterial, inflammation, lung, Th1/Th2 cells |
Academic Unit: | Faculty of Science and Engineering > Biology Faculty of Science and Engineering > Research Institutes > Institute of Immunology |
Item ID: | 311 |
Depositing User: | Bernard Mahon |
Date Deposited: | 14 Jun 2006 |
Journal or Publication Title: | Clinical and Experimental Allergy |
Publisher: | Blackwell Publishing |
Refereed: | Yes |
Related URLs: | |
URI: | https://mural.maynoothuniversity.ie/id/eprint/311 |
Use Licence: | This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available here |
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