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Tumour necrosis factor (TNFα) as a novel therapeutic target in symptomatic corticosteroid dependent asthma

Tumour necrosis factor (TNFα) as a novel therapeutic target in symptomatic corticosteroid dependent asthma
Tumour necrosis factor (TNFα) as a novel therapeutic target in symptomatic corticosteroid dependent asthma
Background: Tumour necrosis factor {alpha} (TNF{alpha}) is a major therapeutic target in a range of chronic inflammatory disorders characterised by a Th1 type immune response in which TNF{alpha} is generated in excess. By contrast, asthma is regarded as a Th2 type disorder, especially when associated with atopy. However, as asthma becomes more severe and chronic, it adopts additional characteristics including corticosteroid refractoriness and involvement of neutrophils suggestive of an altered inflammatory profile towards a Th1 type response, incriminating cytokines such as TNF{alpha}.
Methods: TNF{alpha} levels in bronchoalveolar lavage (BAL) fluid of 26 healthy controls, 42 subjects with mild asthma and 20 with severe asthma were measured by immunoassay, and TNF{alpha} gene expression was determined in endobronchial biopsy specimens from 14 patients with mild asthma and 14 with severe asthma. The cellular localisation of TNF{alpha} was assessed by immunohistochemistry. An open label uncontrolled clinical study was then undertaken in 17 subjects with severe asthma to evaluate the effect of 12 weeks of treatment with the soluble TNF{alpha} receptor-IgG1Fc fusion protein, etanercept.
Results: TNF{alpha} levels in BAL fluid, TNF{alpha} gene expression and TNF{alpha} immunoreative cells were increased in subjects with severe corticosteroid dependent asthma. Etanercept treatment was associated with improvement in asthma symptoms, lung function, and bronchial hyperresponsiveness.
Conclusions: These findings may be of clinical significance in identifying TNF{alpha} as a new therapeutic target in subjects with severe asthma. The effects of anti-TNF treatment now require confirmation in placebo controlled studies.
asthma, tumour necrosis factor alpha (TNF{alpha}), bronchial hyperresponsiveness, etanercept, corticosteroid
0040-6376
1012-1018
Howarth, P.H.
ff19c8c4-86b0-4a88-8f76-b3d87f142a21
Babu, K.S.
b21f201e-3285-4943-9347-a1a3c8727a00
Arshad, H.S.
debe35ce-76f3-4471-b9f0-9015ff7e5e4c
Lau, L.
2af8045d-6162-4939-aba7-28dd2f60f6a8
Buckley, M.
0a782ca9-25c4-4b3f-b08a-ca678bfbbc69
McConnell, W.
751ac7e8-4904-4d8e-ba44-6430c0e2ff86
Beckett, P.
e6941413-5df1-43f9-9b8e-77c0ef535182
Ali, M. Al
57503030-5d83-40ec-ad2b-f5ae9a8e7311
Chauhan, A.
8e0ac32a-b41d-44cf-9e17-2395913dfee5
Wilson, S.J.
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Reynolds, A.
fd5d3c46-65a9-48d7-8d5d-f6da349fdb2a
Davies, D.E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Holgate, S.T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Howarth, P.H.
ff19c8c4-86b0-4a88-8f76-b3d87f142a21
Babu, K.S.
b21f201e-3285-4943-9347-a1a3c8727a00
Arshad, H.S.
debe35ce-76f3-4471-b9f0-9015ff7e5e4c
Lau, L.
2af8045d-6162-4939-aba7-28dd2f60f6a8
Buckley, M.
0a782ca9-25c4-4b3f-b08a-ca678bfbbc69
McConnell, W.
751ac7e8-4904-4d8e-ba44-6430c0e2ff86
Beckett, P.
e6941413-5df1-43f9-9b8e-77c0ef535182
Ali, M. Al
57503030-5d83-40ec-ad2b-f5ae9a8e7311
Chauhan, A.
8e0ac32a-b41d-44cf-9e17-2395913dfee5
Wilson, S.J.
21c6875d-6870-441b-ae7a-603562a646b8
Reynolds, A.
fd5d3c46-65a9-48d7-8d5d-f6da349fdb2a
Davies, D.E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Holgate, S.T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc

Howarth, P.H., Babu, K.S., Arshad, H.S., Lau, L., Buckley, M., McConnell, W., Beckett, P., Ali, M. Al, Chauhan, A., Wilson, S.J., Reynolds, A., Davies, D.E. and Holgate, S.T. (2005) Tumour necrosis factor (TNFα) as a novel therapeutic target in symptomatic corticosteroid dependent asthma. Thorax, 60 (12), 1012-1018. (doi:10.1136/thx.2005.045260).

Record type: Article

Abstract

Background: Tumour necrosis factor {alpha} (TNF{alpha}) is a major therapeutic target in a range of chronic inflammatory disorders characterised by a Th1 type immune response in which TNF{alpha} is generated in excess. By contrast, asthma is regarded as a Th2 type disorder, especially when associated with atopy. However, as asthma becomes more severe and chronic, it adopts additional characteristics including corticosteroid refractoriness and involvement of neutrophils suggestive of an altered inflammatory profile towards a Th1 type response, incriminating cytokines such as TNF{alpha}.
Methods: TNF{alpha} levels in bronchoalveolar lavage (BAL) fluid of 26 healthy controls, 42 subjects with mild asthma and 20 with severe asthma were measured by immunoassay, and TNF{alpha} gene expression was determined in endobronchial biopsy specimens from 14 patients with mild asthma and 14 with severe asthma. The cellular localisation of TNF{alpha} was assessed by immunohistochemistry. An open label uncontrolled clinical study was then undertaken in 17 subjects with severe asthma to evaluate the effect of 12 weeks of treatment with the soluble TNF{alpha} receptor-IgG1Fc fusion protein, etanercept.
Results: TNF{alpha} levels in BAL fluid, TNF{alpha} gene expression and TNF{alpha} immunoreative cells were increased in subjects with severe corticosteroid dependent asthma. Etanercept treatment was associated with improvement in asthma symptoms, lung function, and bronchial hyperresponsiveness.
Conclusions: These findings may be of clinical significance in identifying TNF{alpha} as a new therapeutic target in subjects with severe asthma. The effects of anti-TNF treatment now require confirmation in placebo controlled studies.

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e-pub ahead of print date: 15 September 2005
Published date: December 2005
Keywords: asthma, tumour necrosis factor alpha (TNF{alpha}), bronchial hyperresponsiveness, etanercept, corticosteroid

Identifiers

Local EPrints ID: 27155
URI: http://eprints.soton.ac.uk/id/eprint/27155
ISSN: 0040-6376
PURE UUID: f9a46fca-ec50-4fa0-9560-6e80cbc658c0
ORCID for S.J. Wilson: ORCID iD orcid.org/0000-0003-1305-8271
ORCID for D.E. Davies: ORCID iD orcid.org/0000-0002-5117-2991

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Date deposited: 26 Apr 2006
Last modified: 16 Mar 2024 02:34

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Contributors

Author: P.H. Howarth
Author: K.S. Babu
Author: H.S. Arshad
Author: L. Lau
Author: M. Buckley
Author: W. McConnell
Author: P. Beckett
Author: M. Al Ali
Author: A. Chauhan
Author: S.J. Wilson ORCID iD
Author: A. Reynolds
Author: D.E. Davies ORCID iD
Author: S.T. Holgate

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