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Attachment of columnar airway epithelial cells in asthma
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
2005 (English)In: Tissue & Cell, ISSN 0040-8166, E-ISSN 1532-3072, Vol. 37, no 2, 145-152 p.Article in journal (Refereed) Published
Abstract [en]

Shedding of airway epithelial cells is a common finding in asthma. In this study, the attachment of the airway epithelial cells to the basal lamina (BL) was investigated by transmission electron microscopy (TEM) of biopsies from patients with atopic asthma and healthy controls. The following parameters were quantitatively determined: the height of the epithelium and of the columnar cells, the number of basal cells per 100 microm of basal lamina, the contact surfaces of basal cells or columnar cells with the basal lamina, and between basal cells and columnar cells. In order to compare the quantitative method with previous literature data, measurements were also carried out on rat airway epithelium. Compared to the rat, the columnar cell height in the human is increased, basal cells are smaller, and there is a larger contact area between basal cells and basal lamina, as well as between basal and columnar cells. The contact area between columnar cells and basal lamina is hence less in the human airway. The contact area between columnar cells and basal lamina in asthmatics is significantly less than in healthy controls, due to larger intercellular spaces. It is concluded that attachment of columnar cells to the basal lamina occurs mainly indirectly, via desmosomal attachment to basal cells, and that direct attachment of columnar cells to the basal lamina is weakened in asthmatics.

Place, publisher, year, edition, pages
2005. Vol. 37, no 2, 145-152 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-94135DOI: 10.1016/j.tice.2004.12.002PubMedID: 15748741OAI: oai:DiVA.org:uu-94135DiVA: diva2:167885
Note

on behalf of the BHR group 1

Available from: 2006-03-22 Created: 2006-03-22 Last updated: 2017-12-14Bibliographically approved
In thesis
1. Ultrastructural Studies of the Airway Epithelium in Airway Diseases
Open this publication in new window or tab >>Ultrastructural Studies of the Airway Epithelium in Airway Diseases
2006 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Ultrastructural studies of airway epithelium in airway disease are important for diagnosis and understanding the underlying pathology which helps clinicians to improve the patients' treatment.

Airway biopsies from a 5-month old boy with respiratory problems and gastro-oesophageal reflux were studied by transmission electron microscopy (TEM). The tracheal columnar cells showed accumulation of lamellar bodies, indicative of lysosomal storage disease. The patient was diagnosed with Gaucher disease type 2.

Shedding of airway epithelial cells is commonly found in asthma. The attachment of these cells to the basal lamina was investigated by TEM of biopsies from patients with asthma and healthy controls. The contact area between columnar cells and basal lamina in asthmatics was significantly less than in controls. Attachment of columnar cells to the basal lamina occurs mainly indirectly, via desmosomal attachment to basal cells.

Primary ciliary dyskinesia (PCD) is a congenital disease. It is important to differentiate PCD from acquired (secondary) ciliary dyskinesia (SCD). The number of dynein arms determined by TEM was 1.5 and 1.4 for outer and inner dynein arms, respectively in PCD, versus 7.9 and 5.2 for controls and 8.1 and 5.9 in SCD. Compared to PCD patients, SCD patients have more structurally abnormal cilia. A significant difference was found in orientation of the central microtubule pair between PCD and SCD, but also overlap.

Leukotriene receptor antagonists are a new treatment for asthma. Both corticosteroids and montelukast caused apoptosis and necrosis of airway epithelial cells, and reduced the expression of intercellular adhesion molecule-1. Treatment of cells with tumor necrosis factor-α or interferon-γ reduced the fraction of the lateral cell membrane occupied by desmosomes and this effect was counteracted by corticosteroids.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2006. 81 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 123
Keyword
Morphology, asthma, cilia, corticosteroids, cytokines, desmosomes, Gaucher’s disease, montelukast, primary ciliary dyskinesia, transmission electron microscopy, Morfologi
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-6632 (URN)91-554-6492-0 (ISBN)
Public defence
2006-04-12, Rosénsalen, Ingång 96, Akademiska Sjukhuset, Uppsala, 13:15
Opponent
Supervisors
Available from: 2006-03-22 Created: 2006-03-22Bibliographically approved
2. 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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