A pinboard by
Endre Szvetnik

I write for Sparrho and work with Curators to translate and disseminate research to the public.

I believe scientific thinking fosters progress and is beneficial to society.


Research into newly found stem cells that can trigger a repair mechanism in damaged lungs.

Researchers have discovered stem cells in the lungs that can repair damaged air sacks. Activating the mechanism can lead to new therapies for severe conditions like chronic obstructive pulmonary disease (COPD).

In 10 seconds? Scientists are studying how to trigger special stem cells found in our lungs to repair tissue, potentially reversing the damage caused by currently incurable COPD.

How did they found those stem cells? Researchers discovered alveolar epithelial progenitor (AEP) cells in the lungs of mice. They found that after infecting the animals with flu, AEP cells quickly expanded and regenerated damaged air-sacs known as alveoli. They then discovered similar stem cells in humans, which make animal studies very valuable to us. Read the research paper

What will these studies lead to? We hope to be able to manipulate this mechanism to help COPD-patients, who have difficulties with breathing. Switching on the process would make the stem cells repair the alveoli, crucial to the oxygen supply of the body.

So, how does the process work? This part of the lung is wrapped in a film of so-called epithelial cells. The same type of cells are present elsewhere in the body protecting cavities. But, whereas in the intestines they renew around every five days, in the lungs renewal only starts when stem cells kick in upon injury. Being able to flick the swith would speed up the healing process, making people breathe more easily.

Is there another way? Scientists have grown epthelial cells in the lab to experiment with artificial scaffolds in order to speed up tissue growth. They are also studying the effects of proteins secreted by nasal fibroblast cells - as such cells play a key role in wound healing.

So, would this be a cure for COPD? These are only the first, but promising steps. Epithelial cells are vital for healthy airway functions, so the discovery could lead to therapies not only for COPD but for cystic fibrosis as well. And as the respiratory and vascular systems are closely linked, scientists want to use the method for blood vessel regeneration.

Why do we need to talk about COPD?

Chronic obstructive pulmonary disease is expected to become the 3rd leading cause of death worldwide by 2030, with over 60 million people living with the condition around the globe.

COPD - which is mainly caused by smoking - gets worse over time and has no cure, but can be managed by the right treatment.

It is accompanied by lung damage in the alveoli, that results in less oxygen reaching parts of the body, with less carbon dioxide being exhaled.

This results in symptoms such as shortness of breath, coughing, mucus production and wheezing.


Epithelial cell-extracellular matrix interactions and stem cells in airway epithelial regeneration.

Abstract: In healthy subjects, the respiratory epithelium forms a continuous lining to the airways and to the environment, and plays a unique role as a barrier against external deleterious agents to protect the airways from the insults. In respiratory diseases such as cystic fibrosis (CF), chronic obstructive pulmonary disease (COPD), chronic bronchitis, or asthma, the airway epithelium is frequently remodeled and injured, leading to the impairment of its defense functions. The rapid restoration of the epithelial barrier is crucial for these patients. The complete regeneration of the airway epithelium is a complex phenomenon, including not only the epithelial wound repair but also the epithelial differentiation to reconstitute a fully well differentiated and functional epithelium. The regeneration implies two partners: the epithelial stem/progenitor cells and factors able to regulate this process. Among these factors, epithelial cells-extracellular matrix (ECM) interactions play a crucial role. The secretion of a provisional ECM, the cell-ECM relationships through epithelial receptors, and the remodeling of the ECM by proteases (mainly matrix metalloproteinases) contribute not only to airway epithelial repair by modulating epithelial cell migration and proliferation, but also to the differentiation of repairing cells leading to the complete restoration of the wounded epithelium. A better characterization of resident stem cells and of effectors of the regeneration process is an essential prerequisite to propose new regenerative therapeutics to patients suffering from infectious/inflammatory respiratory diseases.

Pub.: 08 Aug '08, Pinned: 13 Jun '18

[Repair and regeneration of the airway epithelium].

Abstract: Despite an efficient defence system, the airway surface epithelium, in permanent contact with the external milieu, is frequently injured by inhaled pollutants, microorganisms and viruses. The response of the airway surface epithelium to an acute injury includes a succession of cellular events varying from the loss of the surface epithelium integrity to partial shedding of the epithelium or even to complete denudation of the basement membrane. The epithelium has then to repair and regenerate to restore its functions, through several mechanisms including basal cell spreading and migration, followed by proliferation and differentiation of epithelial cells. The cellular and molecular factors involved in wound repair and epithelial regeneration are closely interacting and imply extracellular matrix proteins, matrix metalloproteinases (MMPs) and their inhibitors as well as cytokines and growth factors secreted by airway epithelial and mesenchymal cells. The development of in vitro and in vivo models of airway epithelium wound repair allowed the study of the spatio-temporal modulation of these factors during the different steps of epithelial repair and regeneration. In this context, several studies have demonstrated that the matrix and secretory environment are markedly involved in these mechanisms and that their dysregulation may induce remodelling of the airway mucosa. A better knowledge of the mechanisms involved in airway epithelium regeneration may pave the way to regenerative therapeutics allowing the reconstitution of a functional airway epithelium in numerous respiratory diseases such as asthma, chronic obstructive pulmonary diseases, cystic fibrosis and bronchiolitis.

Pub.: 06 Dec '05, Pinned: 13 Jun '18

Airway epithelial repair, regeneration, and remodeling after injury in chronic obstructive pulmonary disease.

Abstract: In chronic obstructive pulmonary disease (COPD), exacerbations are generally associated with several causes, including pollutants, viruses, bacteria that are responsible for an excess of inflammatory mediators, and proinflammatory cytokines released by activated epithelial and inflammatory cells. The normal response of the airway surface epithelium to injury includes a succession of cellular events, varying from the loss of the surface epithelium integrity to partial shedding of the epithelium or even complete denudation of the basement membrane. The epithelium then has to repair and regenerate to restore its functions, through several mechanisms, including basal cell spreading and migration, followed by proliferation and differentiation of epithelial cells. In COPD, the remodeling of the airway epithelium, such as squamous metaplasia and mucous hyperplasia that occur during injury, may considerably disturb the innate immune functions of the airway epithelium. In vitro and in vivo models of airway epithelial wound repair and regeneration allow the study of the spatiotemporal modulation of cellular and molecular interaction factors-namely, the proinflammatory cytokines, the matrix metalloproteinases and their inhibitors, and the intercellular adhesion molecules. These factors may be markedly altered during exacerbation periods of COPD and their dysregulation may induce remodeling of the airway mucosa and a leakiness of the airway surface epithelium. More knowledge of the mechanisms involved in airway epithelium regeneration may pave the way to cytoprotective and regenerative therapeutics, allowing the reconstitution of a functional, well-differentiated airway epithelium in COPD.

Pub.: 27 Oct '06, Pinned: 13 Jun '18