The University of Southampton
University of Southampton Institutional Repository

Enhancement of neutrophil function by the bronchial epithelium stimulated by EGF

Enhancement of neutrophil function by the bronchial epithelium stimulated by EGF
Enhancement of neutrophil function by the bronchial epithelium stimulated by EGF
The bronchial epithelium is an important physical barrier that also regulates physiological processes including leukocyte trafficking. We aimed to elucidate the mechanisms whereby the bronchial epithelium, stimulated by epidermal growth factor (EGF) as part of a response to acute or chronic injury, could activate and chemoattract human neutrophils.Sub-confluent 16HBE cells were stimulated with EGF to mimic what happens in vivo after injury. The effect of the resulting conditioned media (EGF-CM) was compared with that of basal conditioned media (basal-CM) in respect of neutrophil activation and chemotaxis. Such findings were then confirmed using primary bronchial epithelial cells (PBECs) from healthy volunteers.EGF-CM from 16HBE cells caused increased expression of CD11b/CD66b and CD62L loss on neutrophils when compared to basal-CM. EGF-CM contained significant neutrophil chemotactic activity involving GM-CSF and IL-8 that was potentiated by LTB4. This was dependent on neutrophil PI3K activation and Akt phosphorylation, with partial regulation by PLD, but not mTOR. Consistent with these observations, EGF-CM derived from PBECs displayed increased chemotactic activity.Our results suggest that the enhanced chemotactic activity of the EGF-conditioned epithelium can enhance neutrophil-mediated immunity during acute injury, while during continued injury and repair, as in chronic asthma, this could contribute to persistent neutrophilic inflammation.
0903-1936
714-724
Uddin, M.
4b66ec3d-6584-46e5-8cf0-e7a9e975e5e5
Seumois, G.
fa404dbb-42e3-47a2-9479-cc5c34c61086
Lau, L.C.
2af8045d-6162-4939-aba7-28dd2f60f6a8
Rytila, P.
397559b3-550c-4bb4-bac7-f49735ce51d2
Davies, D.E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Djukanovic, R.
d9a45ee7-6a80-4d84-a0ed-10962660a98d
Uddin, M.
4b66ec3d-6584-46e5-8cf0-e7a9e975e5e5
Seumois, G.
fa404dbb-42e3-47a2-9479-cc5c34c61086
Lau, L.C.
2af8045d-6162-4939-aba7-28dd2f60f6a8
Rytila, P.
397559b3-550c-4bb4-bac7-f49735ce51d2
Davies, D.E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Djukanovic, R.
d9a45ee7-6a80-4d84-a0ed-10962660a98d

Uddin, M., Seumois, G., Lau, L.C., Rytila, P., Davies, D.E. and Djukanovic, R. (2008) Enhancement of neutrophil function by the bronchial epithelium stimulated by EGF. European Respiratory Journal, 31 (4), 714-724. (doi:10.1183/09031936.00144307). (PMID:18094008)

Record type: Article

Abstract

The bronchial epithelium is an important physical barrier that also regulates physiological processes including leukocyte trafficking. We aimed to elucidate the mechanisms whereby the bronchial epithelium, stimulated by epidermal growth factor (EGF) as part of a response to acute or chronic injury, could activate and chemoattract human neutrophils.Sub-confluent 16HBE cells were stimulated with EGF to mimic what happens in vivo after injury. The effect of the resulting conditioned media (EGF-CM) was compared with that of basal conditioned media (basal-CM) in respect of neutrophil activation and chemotaxis. Such findings were then confirmed using primary bronchial epithelial cells (PBECs) from healthy volunteers.EGF-CM from 16HBE cells caused increased expression of CD11b/CD66b and CD62L loss on neutrophils when compared to basal-CM. EGF-CM contained significant neutrophil chemotactic activity involving GM-CSF and IL-8 that was potentiated by LTB4. This was dependent on neutrophil PI3K activation and Akt phosphorylation, with partial regulation by PLD, but not mTOR. Consistent with these observations, EGF-CM derived from PBECs displayed increased chemotactic activity.Our results suggest that the enhanced chemotactic activity of the EGF-conditioned epithelium can enhance neutrophil-mediated immunity during acute injury, while during continued injury and repair, as in chronic asthma, this could contribute to persistent neutrophilic inflammation.

This record has no associated files available for download.

More information

e-pub ahead of print date: 19 December 2007
Published date: 1 April 2008
Organisations: Infection Inflammation & Immunity

Identifiers

Local EPrints ID: 59420
URI: http://eprints.soton.ac.uk/id/eprint/59420
ISSN: 0903-1936
PURE UUID: 0a7e03e4-3fba-4c84-813c-ade43d4fd6e3
ORCID for D.E. Davies: ORCID iD orcid.org/0000-0002-5117-2991
ORCID for R. Djukanovic: ORCID iD orcid.org/0000-0001-6039-5612

Catalogue record

Date deposited: 03 Sep 2008
Last modified: 16 Mar 2024 02:36

Export record

Altmetrics

Contributors

Author: M. Uddin
Author: G. Seumois
Author: L.C. Lau
Author: P. Rytila
Author: D.E. Davies ORCID iD
Author: R. Djukanovic ORCID iD

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×