The relation between connective tissue cells and intercellular substances, including basement membranes

Our plain-English summary of The relation between connective tissue cells and intercellular substances, including basement membranes, by P. Davies, A.C. Allison, C.J. Cardella (Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences, 1975).

The study

• Authors: P. Davies, A.C. Allison, C.J. Cardella
• Journal: Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
• Published: 1975;271(912):363-77
• Cited by: 4 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Basement membranes are distributed widely in the body forming an extracellular matrix for epithelial and endothelial cells. The collagenous and glycoprotein constituents of basement membranes are synthesized by these two cell types. Disturbance of the interactions between basement membranes and their associated epithelial and endothelial cells can lead to the pathological changes seen in diseases involving basement membranes. These changes are illustrated here by reference to glomerulonephritis induced by the deposition of immune complexes in the glomerulus of the kidney, and chronic inflammatory changes occurring in the lung after inhalation of asbestos. In these diseases basement membrane changes can occur in several ways. Hydrolytic enzymes released from inflammatory cells degrade basement membranes while other constituents by epithelial and endothelial cells. Alternatively the physical separation of epithelial and endothelial cells from their basement membrances by space-occupying substances such as immune complexes can interfere with feedback mechanisms leading to synthesis of basement membrane constituents and cell proliferation. Studies of these pathological changes at a cellular level should shed new light on the ways in which cells interact with their pericellular environment.

In plain English

This 1975 paper was mainly a review and discussion of how cells interact with basement membranes, the thin sheets that support lining cells. The authors used two examples: kidney disease caused by immune complexes, and lung changes after asbestos inhalation. They also reported their own laboratory experiments. Mouse peritoneal mononuclear phagocytes (scavenger cells) were grown in dishes and exposed to chrysotile asbestos (U.I.C.C. Chrysotile A). The authors found that small amounts of asbestos released large quantities of lysosomal enzymes from the cells, rising with the asbestos concentration, without detectable loss of cell viability. Lactate dehydrogenase, a marker of cell damage, was not released. At 50 micrograms per millilitre, after a lag of about 3 hours, 62.8 plus or minus 1.7 % of one enzyme's activity was in the culture medium by 24 hours, compared with 22.9 plus or minus 3.5 % in control cultures. The authors suggested that similar release in the lung would produce enzymes that damage alveolar basement membranes. They concluded that certain pathological changes in diseases involving the kidney and the lung result from disturbing a delicate balance that normally exists between cells and their surroundings.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Review and discussion paper, including the authors' own laboratory (cell culture) experiments with asbestos
• Who was studied: Mouse peritoneal mononuclear phagocytes in culture (number of cultures not stated)
• Exposure: Chrysotile asbestos (U.I.C.C. Chrysotile A) at various concentrations for 24 h, and at 50 μg/ml over a time course of up to 24 h
• Main results:
  • Small amounts of asbestos released large quantities of acid hydrolases (lysosomal enzymes) from mononuclear phagocytes
  • The release occurred without any detectable loss of cell viability
  • In cells exposed for 24 h, lysosomal enzyme activity in the culture medium increased with asbestos concentration
  • Lactate dehydrogenase, a marker of cell damage, was not released at any asbestos concentration used
  • Cellular levels of lactate dehydrogenase increased significantly in cultures exposed to more than 2 μg/ml asbestos
  • Enzyme release began after an initial lag period of 3 h
  • In cultures exposed to asbestos at 50 μg/ml, 62.8 ± 1.7 % of total enzyme activity was in the culture medium by 24 h, compared with 22.9 ± 3.5 % in control cultures
• The authors' conclusion: The authors concluded that certain pathological changes in diseases involving the kidney and the lung result from disturbing a normal balance between cells and their surroundings. They proposed that, if similar enzyme release occurred in the lung after asbestos inhalation, it would release enzymes that damage alveolar basement membranes.
• Limitations the authors state:
  • For the kidney part of the paper, the authors state that glomerular mesangial cells could not yet be isolated, so their reactivity could not be analysed directly

Topics

Medical terms in this study, explained in our Lexicon: Glycoprotein, Deposition.

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