The effects of theophylline on mucosal inflammation in asthmatic airways: biopsy results
The effects of theophylline on mucosal inflammation in asthmatic airways: biopsy results
Theophylline, a nonspecific phosphodiesterase inhibitor, has only recently been reconsidered as a potential anti-inflammatory drug. Its ability to inhibit late asthmatic responses has pointed to possible inhibition of mechanisms regulating the influx and activity of inflammatory cells into the airways. Increasing evidence points to an anti-inflammatory action of theophylline at doses lower than those necessary for a bronchodilator effect. Withdrawal of theophylline from regular treatment results in an increase both in CD4+ and CD8+ T-cells in the bronchial mucosa and a concomitant decrease in the blood, suggesting that theophylline prevents T-cell trafficking from blood into the airways. Furthermore, pretreatment with theophylline significantly attenuates the influx of eosinophils into the airways associated with an allergen-induced late asthmatic response. In keeping with these observations, in a double-blind, placebo-controlled trial involving mild to moderately severe atopic asthmatics, treatment with theophylline resulted in a significant reduction in the numbers of epithelial CD8+ T-cells. In addition, the numbers of cells containing cytokines, interleukin 4 and 5 (IL-4 and IL-5), decreased in the theophylline-treated group and increased in the placebo-treated group, with the difference between the changes being significant. It would, therefore, appear that theophylline may contribute to asthma control due to its ability to reduce the suppressor/cytotoxic T-cells and cytokines which are relevant to allergic mucosal responses.
831-833
Djukanović, R.
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Finnerty, J.P.
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Lee, C.
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Wilson, S.J.
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Madden, J.
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Holgate, S.T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
May 1995
Djukanović, R.
d9a45ee7-6a80-4d84-a0ed-10962660a98d
Finnerty, J.P.
bb6b2e86-02e0-402c-875a-7c7359cc79a8
Lee, C.
774e8767-13f8-4725-bc9f-c1200ccd78ab
Wilson, S.J.
21c6875d-6870-441b-ae7a-603562a646b8
Madden, J.
0771e352-d432-41ea-8a7e-4704c1efca46
Holgate, S.T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Djukanović, R., Finnerty, J.P., Lee, C., Wilson, S.J., Madden, J. and Holgate, S.T.
(1995)
The effects of theophylline on mucosal inflammation in asthmatic airways: biopsy results.
European Respiratory Journal, 8 (5), .
(doi:10.1183/09031936.95.08050831).
(PMID:7656958)
Abstract
Theophylline, a nonspecific phosphodiesterase inhibitor, has only recently been reconsidered as a potential anti-inflammatory drug. Its ability to inhibit late asthmatic responses has pointed to possible inhibition of mechanisms regulating the influx and activity of inflammatory cells into the airways. Increasing evidence points to an anti-inflammatory action of theophylline at doses lower than those necessary for a bronchodilator effect. Withdrawal of theophylline from regular treatment results in an increase both in CD4+ and CD8+ T-cells in the bronchial mucosa and a concomitant decrease in the blood, suggesting that theophylline prevents T-cell trafficking from blood into the airways. Furthermore, pretreatment with theophylline significantly attenuates the influx of eosinophils into the airways associated with an allergen-induced late asthmatic response. In keeping with these observations, in a double-blind, placebo-controlled trial involving mild to moderately severe atopic asthmatics, treatment with theophylline resulted in a significant reduction in the numbers of epithelial CD8+ T-cells. In addition, the numbers of cells containing cytokines, interleukin 4 and 5 (IL-4 and IL-5), decreased in the theophylline-treated group and increased in the placebo-treated group, with the difference between the changes being significant. It would, therefore, appear that theophylline may contribute to asthma control due to its ability to reduce the suppressor/cytotoxic T-cells and cytokines which are relevant to allergic mucosal responses.
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Published date: May 1995
Organisations:
Infection Inflammation & Immunity
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Local EPrints ID: 190963
URI: http://eprints.soton.ac.uk/id/eprint/190963
ISSN: 0903-1936
PURE UUID: d2873fef-e4f2-4451-8df6-89ed5e09625a
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Date deposited: 21 Jun 2011 09:13
Last modified: 15 Mar 2024 02:36
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Author:
J.P. Finnerty
Author:
C. Lee
Author:
J. Madden
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