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Airway hyperresponsiveness in mouse models of asthma is associated with activated T cells in the airways

Zosky, G.R., Larcombe, A.N., Burchell, J.T., Wikstrom, M.E., Stumbles, P.A., Sly, P.D. and Turner, D.J. (2008) Airway hyperresponsiveness in mouse models of asthma is associated with activated T cells in the airways. In: TSANZ & ANZSRS Annual Scientific Meetings, 28 March - 2 April, Melbourne, Australia


Adoptive transfer of activated T cells has been shown to induce allergic responses in the lung, however, direct physiological evidence of whether these T cells home to the airways is lacking. This study aimed to determine the role of CD4+ T cells in the generation of airway hyperresponsiveness (AHR) in mouse models of asthma.

Methods: (1) 129/Sv, C57BL/6 and BALB/c mice were sensitized and challenged with ovalbumin (OVA). AHR, inflammatory cells, serum IgE and IgG1 and the number of CD4+ CD69+ T cells in the trachea and peripheral lung were measured. (2) DO11.10 transgenic T cells that recognize OVAwere transferred to naïve BALB/c recipients. Recipient mice were primed and challenged with OVAand assessed forAHR and serum antibodies. (3) Naïve BALB/c mice were passively sensitized with high titre IgE/IgG1 titre serum, challenged with OVA and assessed for AHR.

Results: (1) AHR to inhaled methacholine (MCh) was induced by OVA in BALB/c mice only. This correlated with the presence of CD4+ CD69+ T cells and IgG1 . (2) After 5 OVA challenges naïve BALB/c mice primed with DO11.10 T cells demonstrated AHR (p=0.049) to MCh. (3) Passive transfer of high titre IgE/IgG1 serum did not result in AHR.

Conclusions: The presence of AHR in BALB/c mice was linked to the numbers of CD4+ CD69+ T cells and IgG1. Adoptive transfer of T cells that recognize OVA resulted in AHR following challenge suggesting that these T cells traffic to the airway after challenge. This could not be replicated by passively sensitizing mice with high IgE/IgG1 titre serum alone. This study highlighted the potential role of CD4+ T cells in the development of AHR and further studies using this system may be able to dissect the mechanism by which this occurs.

Item Type: Conference Paper
Murdoch Affiliation(s): School of Veterinary and Biomedical Sciences
Notes: Abstract in: Respirology 13 Suppl 2: A15., 2008
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