New Hope for COPD Patients: A Saccharide-Based Treatment That Could Reduce the Effects of Emphysema
With the help of a new mouse model, scientists have recently managed to find a sugar molecule that could have the potential of reducing the progress of emphysema and significantly diminish the negative effects of COPD (chronic obstructive pulmonary disease). Naoyuki Taniguchi, the main scientist leading the experiments at the RIKEN-Max Planck Joint Research Center for Systems Chemical Biology, claims the discovery could later lead to better treatment for several diseases similar to COPD.
Can Sugar Affect the Lungs?
COPD is the fourth deadliest disease worldwide, and Taniguchi’s team worked tirelessly to explore the possibilities linked to the study of a negatively charged sugar molecule that is located in the small airway of the lung. Keratan sulfate, by its scientific name, is a large saccharide found to diminish in mice that were exposed to cigarette smoke. The scientists’ theory is that the decrease could be associated in some way with the mechanism through which smoking damages the lung. The subsequent studies, therefore, became of prime importance in determining whether or not glycan-based treatments for combating emphysema were possible.
An Experiment with Keteran Sulfate
To check whether or not keratan sulfate could be playing 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 triggered by an enzyme named elastase, and which showed clearly that the small air sacs in the lungs, also known as alveoli, were protected as a result of using L4. Further tests suggested that the infiltration of neutrophils – a white blood cell usually released as a response to inflammatory actions – was also reduced, although its production was not halted.
Unfortunately, L4 was not able to prevent, or directly reduce, the release of high levels of inflammatory cytokines and enzymes that are harmful to the lung’s tissue. A slight inhibition was obtained, however, the scientists were forced to conclude that the production of cytokines was also done indirectly, through various other mechanisms related to the neutrophils.
Further Results with the Second Model
In the second experiment, Taniguchi’s team induced emphysema through the process started by a toxin found in bacterial cell walls known as LPS. This model responded differently with the administration of L4, preventing the release of neutrophils entirely. Taniguchi remarked that the saccharide compound was just as effective as dexamethasone, the current steroid-based treatment used for COPD. However, the difference was that, while dexamethasone reduced the neutrophil influx at high risk, involving several debilitating side effects, L4 did not seem to harm the mice in any way, even when administered at higher dosages.
Despite the exciting results, the scientists were quick to point out that much work still remains to be done. The method through which L4 manages to prevent neutrophil activity is still more or less unknown, and a target receptor protein has not yet been found. However, with L4 now being capable to reduce inflammation without any other special measures needing to be taken, there is far more hope than ever before in finding a viable treatment for COPD that is completely free of any unwanted side effects.