Reducing The Effects Of Emphysema
Using a new mouse model, scientists have recently succeeded in finding a sugar molecule that has the ability to reduce the progress of emphysema and significantly reduce the negative effects of COPD (chronic obstructive pulmonary disease). Naoyuki Taniguchi, the lead scientist who led the experiments at the RIKEN-Max Planck Joint Research Center for Systems Chemical Biology, claims that the discovery could later lead to better treatment of various diseases similar to COPD.
Can sugar affect the lungs?
COPD is the fourth most deadly disease worldwide and Taniguchi's team worked tirelessly to investigate the possibilities associated with the study of a negatively charged sugar molecule in the small airway of the lung. Keratan sulphate is, according to its scientific name, a large saccharide that has been shown to decrease in mice exposed to cigarette smoke. The scientists' theory is that the decrease can in one way or another be related to the mechanism by which smoking damages the lung. The subsequent studies were therefore of the utmost importance in determining whether or not glycan-based treatments for fighting emphysema were possible.
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An experiment with Keteran sulfate
To check whether keratan sulfate could or did not play a protective role, a repeating disaccharide element was prepared from keratan sulfate. The compound, simply known as L4, would then be administered to two mouse models. The first experiment involved a mouse model in which emphysema was caused by an enzyme called elastase, which clearly showed that the small air pockets in the lungs, also known as alveoli, were protected as a result of the use of L4. Further tests suggested that the infiltration of neutrophils - a white blood cell usually released in response to inflammatory reactions - was also reduced, although production was not stopped.
Unfortunately, L4 was unable to prevent or directly reduce the release of high levels of inflammatory cytokines and enzymes that are harmful to the lung tissue. A slight inhibition was obtained, but the scientists were forced to conclude that the production of cytokines was also performed indirectly, via various other mechanisms related to the neutrophils.
Further results with the second model
In the second experiment, Taniguchi's team induced emphysema by the process that started with a toxin found in bacterial cell walls, known as LPS. This model reacted differently with the administration of L4, thus completely preventing the release of neutrophils. Taniguchi noted that the saccharide compound was as effective as dexamethasone, the current treatment based on steroids used for COPD. However, the difference was that while dexamethasone reduced the influx of high-risk neutrophils with various attenuating side effects, L4 in no way caused any damage, even at higher doses.
Despite the exciting results, the scientists soon found out that there is still a lot of work to be done. The method by which L4 succeeds in preventing neutrophilic activity is still more or less unknown, and a target receptor protein has not yet been found. Now that L4 is now able to reduce inflammation without taking any other special measures, there is much more hope than ever before in finding a viable treatment for COPD that is completely free of unwanted side effects.
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