#COPD – BioQuakes

In the 19th century, a tuberculosis outbreak killed every one in seven people worldwide. Scientists believed it to be a genetic disease that mainly children developed making it known as “the robber of youth”. It wasn’t until the year 1882 that Robert Koch’s discovery of tubercule bacillus revealed that tuberculosis was not a genetic disease but highly contagious. Although there was some hesitation in the medical community at first, Koch’s findings helped the U.S. launch massive public health campaigns to educate the public on tuberculosis prevention and treatment. Later in 1904, “William Osler and William Welch, together with Edward Livingston Trudeau, founded the forerunner of the American Thoracic Society, the National Association for the Study and Prevention of Tuberculosis”. This sparked the beginning of pulmonary research – the conduction of clinically-oriented research into diseases and disorders affecting the lungs and respiratory tract (including molecular and cell-based investigations). With pulmonary research being around for more than 10o years, one would believe discovering something new at this point in history would be a long shot. But, recently researchers at the Perelman School of Medicine at the University of Pennsylvania found RASCs.

RASCs, also known as respiratory airway secretory cells, “line tiny airway branches, deep in the lungs, near the alveoli structures where oxygen is exchanged for carbon dioxide.” Scientists found that RASCs have stem-cell-like properties that allow them to regenerate other cells that are essential for normal functioning alveoli. They also discovered that smoking and the common smoking-related ailment called chronic obstructive pulmonary disease can disrupt the regenerative functions of RASCs. COPD is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. Emphysema and chronic bronchitis are the two most common conditions that contribute to COPD (both bronchitis and emphysema affect the alveoli, the air sacks of the lungs). The study’s first author Maria Basil, states “COPD is a devastating and common disease, yet we really don’t understand the cellular biology of why or how some patients develop it. Identifying new cell types, in particular new progenitor cells, that are injured in COPD could really accelerate the development of new treatments,”. COPD causes around 3 million deaths worldwide and current treatments can only slow the disease down rather than stop or reverse it. Mice being the common test subjects in lab procedures lack key features of the human lungs, which leads scientists to use healthy human donors to discover RASCs. Since RASCs are secretory cells it means that they produce proteins needed for the fluid lining of the airway. An organelle that we know produces secretory proteins is the ribosome. Ribosomes are tiny organelles that contain RNA and specific proteins within the cytoplasm. Ribosomes are directly involved in the manufacture of proteins by using RNA and amino acids. The discovery of RASCs will not only help advance future COPD treatments but can also lead to discover ways to treat other lung dieases.

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.

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: #COPD

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