In many tissue types there is a reserve of stem cells that is responsible for supporting the healing process after normal inflammation has occurred or an injury has taken place. However, it has not been as widely explored under chronic inflammation conditions. A recent study published in Nature Cell Biology takes a new look at the concept of chronic inflammation and proposes its potential use as a method for new therapies.
The study was conducted by researchers at Ecole polytechnique fédérale de Lausanne (EPFL), described as Europe’s most cosmopolitan technical university with students, professors and staff from over 120 nations. The team of scientists at EPFL’s Swiss Institute for Experimental Cancer Research (ISREC) have discovered that chronic inflammation can lead to metaplasia or the ability for cells to actually change type. In the case of this study, eye cells made a dramatic transformation into skin cells!
Using a corneal epithelium mouse model, chronic inflammation was simulated and the method of fluorescent staining of specific cells was used to help observe and analyze stem cells located in the cornea. Chronic inflammation led to a “stiffer” environment due to the presence of both immune cells and also a substance that causes cells to stick together. The corneal stem cells possess sensors which allow them to sense their environment, make proper adaptations or adjustments and also communicate with other cells. The increased stiffness of their surroundings led the stem cells to not only respond to the changing environment but to actually improperly differentiate.
As a result, instead of differentiating into corneal cells, the faulty programming resulted in the stem cells differentiating into skin cells leading to blindness in the mice. The lead researcher, Freddy Radtke describes the discovery as one that “is relevant to a variety of diseases associated with chronic inflammation, including cancer, and could yield new therapeutic targets.”
Image copyright: Samuel Johnson, flickr CC-BY
Article last time updated on 18.01.2016.