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Asthmatic bronchial epithelium is more susceptible to oxidant-induced apoptosis

Asthmatic bronchial epithelium is more susceptible to oxidant-induced apoptosis
Asthmatic bronchial epithelium is more susceptible to oxidant-induced apoptosis
Abnormal apoptotic mechanisms are associated with disease pathogenesis. Because the asthmatic bronchial epithelium is characteristically damaged with loss of columnar epithelial cells, we postulated that this is due to unscheduled apoptosis. Using an antibody directed toward the caspase cleavage product of poly(ADP-ribose) polymerase, immunohistochemistry applied to endobronchial biopsies showed higher levels of staining in the bronchial epithelium of subjects with asthma as compared with normal control subjects (% epithelial staining [median (range) = 10.5 (1.4–24.5) versus 0.4 (0.0–9.7)]; P < 0.001). Because we were unable to determine whether this difference was due to ongoing inflammation in vivo, cultures of normal and asthmatic bronchial epithelial cells were used to study apoptosis in vitro. In complete growth medium, these cells showed no difference in their rate of proliferation or viability.
However, cells from subjects with asthma were more susceptible to the apoptotic effects of H2O2 than cells from normal control subjects (% apoptotic cells = 32.2 [8.8–54.9] versus 14.3 [6.4–24.7]; P < 0.05), even though both were similarly affected by treatment with actinomycin D. These data indicate that the susceptibility of asthmatic bronchial epithelium to oxidants is greater than normal. This susceptibility may contribute to the rising trends in asthma associated with air pollution and diets low in antioxidants.
1044-1549
179-185
Bucchieri, Fabio
3f85c9c8-2bc0-4fd0-b481-a03935fe3cb0
Puddicombe, Sarah M.
fd8d76d1-203d-4f06-a7c2-678c946fb931
Lordan, James L.
15a9bdfb-bf61-4aea-a0f4-d83868eb39d0
Richter, Audrey
5b4fb888-b3a7-4b81-a8a7-ffd2c046a196
Buchanan, Diane
a30b878e-ca84-48ac-b52d-96a36e78ef74
Wilson, Susan J.
21c6875d-6870-441b-ae7a-603562a646b8
Ward, Jon
d1ec2453-e1f2-47f9-9679-066f798f6cad
Zummo, Giovanni
54897ebe-00d6-47b9-9914-fb350deb7b14
Howarth, Peter H.
ff19c8c4-86b0-4a88-8f76-b3d87f142a21
Djukanovic, Ratko
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Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Davies, Donna E.
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Bucchieri, Fabio
3f85c9c8-2bc0-4fd0-b481-a03935fe3cb0
Puddicombe, Sarah M.
fd8d76d1-203d-4f06-a7c2-678c946fb931
Lordan, James L.
15a9bdfb-bf61-4aea-a0f4-d83868eb39d0
Richter, Audrey
5b4fb888-b3a7-4b81-a8a7-ffd2c046a196
Buchanan, Diane
a30b878e-ca84-48ac-b52d-96a36e78ef74
Wilson, Susan J.
21c6875d-6870-441b-ae7a-603562a646b8
Ward, Jon
d1ec2453-e1f2-47f9-9679-066f798f6cad
Zummo, Giovanni
54897ebe-00d6-47b9-9914-fb350deb7b14
Howarth, Peter H.
ff19c8c4-86b0-4a88-8f76-b3d87f142a21
Djukanovic, Ratko
d9a45ee7-6a80-4d84-a0ed-10962660a98d
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Davies, Donna E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38

Bucchieri, Fabio, Puddicombe, Sarah M., Lordan, James L., Richter, Audrey, Buchanan, Diane, Wilson, Susan J., Ward, Jon, Zummo, Giovanni, Howarth, Peter H., Djukanovic, Ratko, Holgate, Stephen T. and Davies, Donna E. (2002) Asthmatic bronchial epithelium is more susceptible to oxidant-induced apoptosis. American Journal of Respiratory Cell and Molecular Biology, 27 (2), 179-185. (doi:10.1165/ajrcmb.27.2.4699).

Record type: Article

Abstract

Abnormal apoptotic mechanisms are associated with disease pathogenesis. Because the asthmatic bronchial epithelium is characteristically damaged with loss of columnar epithelial cells, we postulated that this is due to unscheduled apoptosis. Using an antibody directed toward the caspase cleavage product of poly(ADP-ribose) polymerase, immunohistochemistry applied to endobronchial biopsies showed higher levels of staining in the bronchial epithelium of subjects with asthma as compared with normal control subjects (% epithelial staining [median (range) = 10.5 (1.4–24.5) versus 0.4 (0.0–9.7)]; P < 0.001). Because we were unable to determine whether this difference was due to ongoing inflammation in vivo, cultures of normal and asthmatic bronchial epithelial cells were used to study apoptosis in vitro. In complete growth medium, these cells showed no difference in their rate of proliferation or viability.
However, cells from subjects with asthma were more susceptible to the apoptotic effects of H2O2 than cells from normal control subjects (% apoptotic cells = 32.2 [8.8–54.9] versus 14.3 [6.4–24.7]; P < 0.05), even though both were similarly affected by treatment with actinomycin D. These data indicate that the susceptibility of asthmatic bronchial epithelium to oxidants is greater than normal. This susceptibility may contribute to the rising trends in asthma associated with air pollution and diets low in antioxidants.

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Published date: 2002

Identifiers

Local EPrints ID: 26970
URI: http://eprints.soton.ac.uk/id/eprint/26970
ISSN: 1044-1549
PURE UUID: 57f20098-eb6a-4090-952a-58db635eea79
ORCID for Susan J. Wilson: ORCID iD orcid.org/0000-0003-1305-8271
ORCID for Ratko Djukanovic: ORCID iD orcid.org/0000-0001-6039-5612
ORCID for Donna E. Davies: ORCID iD orcid.org/0000-0002-5117-2991

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Date deposited: 25 Apr 2006
Last modified: 18 Feb 2021 16:40

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