The Nose Knows: Pungent Compound Associated with Improvements in Atherosclerotic Plaque

A new study reveals that putrescine, a key compound for body decomposition with a noxious smell, could find redemption as a treatment for atherosclerosis and other inflammatory diseases.

“It’s estimated that a billion cells die in the body every day, and if you don’t get rid of them, they can cause inflammation and tissue death,” Dr. Ira Tabas, the Richard J. Stock Professor of Medicine and professor of pathology & cell biology (in physiology & cellular biophysics) at Columbia University Vagelos College of Physicians and Surgeons, said in a press release. “Removing these dead cells by a process called ‘efferocytosis’ (from the Latin ‘to carry to the grave’) is one of the body’s most important functions.”

Putrescine Improves Plaques

The team looked a human microphages and compared them to dying cells in a dish. They observed that macrophages reclaim arginine and other amino acids when they “eat” dead cells, and then use an enzyme to convert arginine to putrescine. The putrescine, in return, activates a protein (Rac1) that causes the macrophage to eat more dead cells, suggesting to the authors that the problem of atherosclerosis may be, in part, a problem of putrescine. When they put the compound in the drinking water of atherosclerotic mice, the observed that the animals’ microphages got better at eating dead cells and produce improved plaque profiles.

The findings, according to the accompanying press release, suggest that the compound could be use to potentially treat conditions with chronic inflammation, such as Alzheimer’s disease.

“Fortunately, when you dissolve putrescine into water, at least at the dosages needed to improve the plaques, it no longer gives off its odor. The mice drank it without any problem and show no signs of sickness,” Dr. Tabas said, whose findings were published in Cell Metabolism. “Of course we do not yet know the feasibility and safety of using low-dose putrescine to ward off atherosclerotic heart disease and other diseases driven by defective efferocytosis. However, the study shows the potential of treating heart disease with compounds that help macrophages eat dead cells and that are currently in clinical trials for other indications.”