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Effect of cytokines on ICAM-1 and ZO-1 expression on human airway epithelial cells.
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Cell Biology.
2005 (English)In: Cell Biol Int, ISSN 1065-6995, Vol. 29, no 9, 768-77 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2005. Vol. 29, no 9, 768-77 p.
Identifiers
URN: urn:nbn:se:uu:diva-79752PubMedID: 16087364OAI: oai:DiVA.org:uu-79752DiVA: diva2:107665
Available from: 2006-04-13 Created: 2006-04-13 Last updated: 2011-01-11
In thesis
1. Cell Contacts and Airway Epithelial Damage in Asthma
Open this publication in new window or tab >>Cell Contacts and Airway Epithelial Damage in Asthma
2005 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Airway epithelial damage is commonly found in asthma patients. Epithelial damage was investigated with special reference to contacts between epithelial cells.

Eosinophils, common in allergic asthma, secrete cationic proteins, particularly major basic protein (MBP). The effect of poly-L-arginine, an analogue of MBP, on airway epithelial cells was investigated. Poly-L-arginine induced membrane damage, resulting in increased permeability, loss of cell-cell contracts (tight junctions and desmosomes) and generalized cell damage.

Adhesion molecules on airway epithelial cells may be important in recruiting leukocytes. Interferon (IFN)-γ increased intracellular adhesion molecule-1 expression in airway epithelial cell lines. A combination of interleukin-4 and IFN-γ opened the tight junctions.

Epithelial damage in asthma was studied at the ultrastructural level in bronchial biopsies from patients with atopic or non-atopic asthma, and healthy controls. Epithelial damage was extensive in both asthma groups. In basal and columnar cells, relative desmosome length was reduced by 30-40%. In columnar cells, half-desmosomes were noticed. Changes tended to be more extensive in atopic asthma, but there was no significant difference between the two groups. Reduced desmosomal contact may be important in the epithelial shedding observed in asthma. The contact area between columnar cells and basal lamina is relatively small in the human airway. Attachment of columnar cells to the basal lamina occurs indirectly, via desmosomal attachment to basal cells. Direct attachment of columnar cells to the basal lamina is weakened in asthmatics.

Nasal polyposis is a chronic inflammatory disease often associated with asthma. An ultrastructural study showed that epithelial damage of columnar cells is more pronounced in allergic patients. The length of columnar cell desmosomes was significantly reduced in asthmatics vs. non-asthmatics, and in allergics vs. non-allergics.

Cell contacts in airway epithelium in asthmatics are weakened, which may be an intrinsic feature or due to the presence of eosinophils producing toxic proteins.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2005. 62 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 5
Keyword
Anatomy, Desmosomes, tight junctions, major basic protein, eosinophil, cytokines, epithelial damage., Anatomi
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-4775 (URN)91-554-6142-5 (ISBN)
Public defence
2005-03-07, B7:113a, BMC, Husargatan 3, Uppsala, 13:15 (English)
Opponent
Supervisors
Available from: 2005-02-14 Created: 2005-02-14 Last updated: 2013-07-24Bibliographically approved

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Makeeva, NataliaRoomans, Godfried M

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