Whenever attempting to (solve) complicated biological issues, especially those relating to disease treatment, typically referring back to the core principles of the biology of cells is an excellent place to start. One instance where tracing our steps back to the basics of cell biology may be the critical step scientists need to make more significant strides would be treating chronic obstructive pulmonary disease (COPD). According to Johns Hopkins Medicine, “COPD is the fourth leading cause of death in the U.S., affecting more the 15 million adults.” (Johns Hopkins Medicine). 
Treating COPD has had scientists stumped left and right at numerous roadblocks. Patients who experience COPD are constrained to one choice, living with it and treating the symptoms. No actual treatment exists to cure or effectively remove the disease from bodies. COPD isn’t necessarily much of a concern for non-smokers; however, smokers make up colossal numbers of our population, therefore discovering new methods to treat or cure COPD remains high.
Often, obscure and unsuspected treatment methods offer the most ideal-even the best results. For COPD, scientists at the Johns Hopkins Medicine School took a different approach than traditional ways- utilizing far simpler cells compared to human cells to better understand the biological structure of the disease and genes that protect against the harmful chemicals of cigarette smoke.
For this experiment, the scientists utilized the Dictyostelium discoideum amoeba, which is commonly studied to better understand cell movement and communication. Briefly describing the experiment, the scientists pumped cigarette smoke into a chamber filled with the specific amoeba cells. Then, engineered amoebas were deployed to identify any genes that influence the effect of cigarette smoke. Fortunately, one family of genes did spark interest in countering the impact of COPD, the adenine nucleotide translocase (ANT) family. This gene is located on the surface of the mitochondria, which, as we’ve learned, produces Adenosine Triphosphate, or simply cell energy. When the ANT gene is highly active, “cells get better at making fuel [ATP], protecting them from the smoke”( Johns Hopkins Medicine). Not only does the ANT gene assist with protecting the amoeba from the smoke, but it also helps them overcome the damaging effects and symptoms caused by cigarette smoke.
While discovering the effects of the ANT gene family on amoeba cells is highly beneficial for our overall understanding, the human application is what ultimately matters. How can we use this newfound knowledge to treat COPD in humans? Well, according to the Johns Hopkins scientists, “To better understand how ANT genes behave in humans, tissue samples of cells lining the lungs were taken from 28 people with COPD who were treated at the University of Pittsburgh and compared the lung cells’ genetic activity with cells from 20 people with normal lung function” (Johns Hopkins Medicine). The scientists learned that COPD patients experienced roughly 20% less of the ANT2 gene’s genetic expression than those with healthy/unaffected lungs. The lead scientist believes that while further research is necessary, producing medicine that increases the amount of the ANT2 gene in COPD patients may be a key component in treating the disease. Hopefully, the damage cigarette smoke has on people’s lungs becomes reversible in the future, and COPD becomes a disease of the past.
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