Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.653876
Title: Studies on the response of pleural leukocytes to asbestos exposure
Author: Li, Xiao Yang
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1992
Availability of Full Text:
Access from EThOS:
Full text unavailable from EThOS. Please try the link below.
Access from Institution:
Abstract:
Exposure to the fibrous silicate mineral, asbestos, is associated with pulmonary fibrosis and lung cancer as well as different types of pleural pathology. The aim of the present study was to assess the pleural leukocyte response to asbestos fibre deposition in the bronchoalveolar space using a rat intratracheal instillation model. Intratracheal heat-killed C.parvum organism was also used to produce pleural inflammation. Normal pleural leukocytes were comprised of macrophages, mast cells, eosinophils and lymphocytes. This population produced urokinase-type plasminogen activator inhibitor (PAI) in culture and contained plasminogen activator intracellularly. Normal pleural leukocytes also released tumor necrosis factor (TNF) and interleukin-1 (IL-1) in culture and the release was enhanced further with LPS stimulation. After intratracheal instillation (I/T) of crocidolite asbestos, pleural leukocyte components were changed with a significant recruitment of macrophages and eosinophils. These populations were found to release increased PAI activity and decreased TNF activity. In contrast, I/T asbestos coupled with other compact mineral dusts considerably increased TNF production by pleural leukocytes. The elaboration of IL-1 by the leukocytes showed an enhanced response to asbestos exposure. In comparison, after I/T asbestos, bronchoalveolar leukocytes produced increased TNF and IL-1 activity in culture. C.parvum induced-pleural inflammation, characterised by substantial recruitment of neutrophils, produced increased PAI activity but decreased TNF and IL-1. During the later stages of the inflammation, the pleural leukocytes released even less TNF and IL-1, but normal levels of PAI.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.653876  DOI: Not available
Share: