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Lab-grown heart cells reveal secrets of “kissing bug” disease

Stanford researchers are using lab-grown heart cells to investigate how Chagas disease, which is spread by "kissing bugs," affects heart health.

You may have heard a buzz of news recently about the spread of the so-called "kissing bug" throughout the United States. Bloodsuckers that prefer to bite sleeping people around the mouth and eyes, the insect is undeniably ugly (you can thank me later for not sharing a picture -- click here if you'd like to take a gander). But more importantly, they can spread a parasite to humans that causes Chagas disease.

People infected with the parasite, called Trypanosoma cruzi, develop (among other symptoms) fever, aches, fatigue, diarrhea and vomiting. About 30 percent of those infected go on to develop chronic Chagas disease, which can cause long-term health complications including heart failure and digestive problems. Varieties of the bug are found in 28 states, mostly in the southern parts of the country. It is widespread in South America, and Chagas disease is estimated to contribute to more than 10,000 deaths each year.

Now cardiologist and stem cell researcher Joseph Wu, MD, PhD, together with visiting scholar Adriana Bozzi, PhD, have used lab-grown heart muscle cells called cardiomyocytes to investigate at a cellular level how the infection spread by the bugs affects cardiac function. They published their findings recently in Stem Cell Reports.

As Wu, who directs the Stanford Cardiovascular Institute, explained in an email to me:

Chagas disease presents as an acute phase that is generally asymptomatic, followed by a lifelong chronic phase affecting the heart muscle. Researchers have tried to use rodents to study the effect on the heart by Chagas disease, but fundamental differences between mice and humans make this approach less than optimal. We thought we could learn valuable insights by using human induced pluripotent cell-derived cardiomyocytes to directly study how infection with T. cruzi affects the function of these cells in a laboratory setting.

The results were illuminating. The researchers found that not only could human heart muscle cells become infected with T. cruzi, but that the infection caused changes in how rapidly the cells beat and how well they synchronized their beating with their neighbors. They also displayed other physiological changes consistent with the negative clinical outcomes seen in people with Chagas disease.

As Wu explained:

We were really intrigued by how closely our model of T. cruzi infection mirrors some aspects of the symptoms observed in patients with Chagas disease. Our study shows that these lab-grown human heart muscle cells are a good model for studying the cardiac dysfunction seen in chronically infected people and exploring new treatment strategies. For example, our study identified a list of relevant genes that might play a role in the damage caused by Chagas disease, which then could be potential targets for pharmacological intervention.

Photo by Angela

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