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The Strathprints institutional repository is a digital archive of University of Strathclyde's Open Access research outputs. Strathprints provides access to thousands of Open Access research papers by University of Strathclyde researchers, including by researchers from the Department of Computer & Information Sciences involved in mathematically structured programming, similarity and metric search, computer security, software systems, combinatronics and digital health.

The Department also includes the iSchool Research Group, which performs leading research into socio-technical phenomena and topics such as information retrieval and information seeking behaviour.


Tumour necrosis factor-α blockade suppresses murine allergic airways inflammation

Hutchison, S. and Choo-Kang, B.S.W. and Bundick, R.V. and Leishman, A.J. and Brewer, J.M. and McInnes, I.B. and Garside, P. (2008) Tumour necrosis factor-α blockade suppresses murine allergic airways inflammation. Clinical and Experimental Immunology, 151 (1). pp. 114-122. ISSN 0009-9104

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Asthma is a heterogeneous disease that has been increasing in incidence throughout western societies and cytokines, including proinflammatory tumour necrosis factor alpha (TNF-a), have been implicated in the pathogenesis of asthma. Anti-TNF-a therapies have been established successfully in the clinic for diseases such as rheumatoid arthritis and Crohn's disease. TNF-ablocking strategies are now being trialled in asthma; however, their mode of action is poorly understood. Based on the observation that TNF-a induces lymph node hypertrophy we have attempted to investigate this as a mechanism of action of TNF-a in airway inflammation by employing twomodels of murine airway inflammation, that we have termed short and long models, representing severe and mild/moderate asthma, respectively. The models differ by their immunization schedules. In the short model, characterized by eosinophilic and neutrophilic airway inflammation the effect of TNF-a blockade was a reduction in draining lymph node (DLN) hypertrophy, eosinophilia, interleukin (IL)-5 production and immunoglobulin E (IgE) production. In the long model, characterized by eosinophilic inflammation, TNF-a blockade produced a reduction in DLN hypertrophy and IL-5 production but had limited effects on eosinophilia and IgE production. These results indicate that anti-TNF-a can suppress DLN hypertrophy and decrease airway inflammation. Further investigations showed that anti-TNF-a-induced inhibition of DLN hypertrophy cannot be explained by preventing l-selectindependent capture of lymphocytes into the DLN. Given that overall TNF blockade was able to suppress the short model (severe) more effectively than the long model (mild/moderate), the results suggest that TNF-a blocking therapies may be more effective in the treatment of severe asthma.