Researchers have identified a possible mechanism for why cutaneous leishmaniasis lesions are painless, an understanding that could lead to the development of new pain medications.
According to a press release from Ohio State University, researchers analyzed leishmaniasis lesions on mouse skin to detect metabolic signalling pathways that differed from uninfected mice.
Their findings suggest the parasites that cause the disease change pain perception.
“No one knows why these lesions are painless—but it has been thought that the parasite somehow manipulates the host physiological system,” said Abhay Satoskar, MD, PhD, senior author of the study and professor of pathology in The Ohio State University College of Medicine, in the release.
“Based on our data, something the parasites do triggers pathways that suppress pain. How they do that, we’re still investigating.”
The authors note that their research both increases understanding of a parasitic disease, it could also lead to the development of new non-narcotic pain medications.
“We hypothesize that any molecules the parasite’s presence is producing could be potential painkillers for other health problems,” Dr. Satoskar said.
The study was published in the journal iScience.
After giving mice chronic infections with Leishmania mexicana, the species that causes cutaneous leishmaniasis in South, Central, and North America, researchers used mass spectrometry analysis of the lesions to identify molecules known to be associated with pain suppression.
They found numerous metabolites that have been linked in previous research to blockage of pain perception. They also found pathways with pain-relief properties tied to the brain’s endocannabinoid system, which is involved in a host of physiological processes, including the pain response.
Cell-culture experiments in infected macrophages, the immune cells in which Leishmania parasites live, showed an increase in most, but not all, of the same changes as in the lesions.
Finding that certain pain-suppression pathways aren’t increased in infected macrophages leaves some questions unanswered, said Dr. Satoskar, who is also a professor of microbiology at Ohio State.
“The infection does something in the cell that could be a direct or indirect effect—we don’t know. But the environment that the infection creates leads to production of these metabolites,” he said. “The exciting thing is that this is the first time we’ve begun to understand the cellular basis of why there is no pain in these lesions.
“The next key question is, if we know these pathways are responsible, then how are they triggered? By the parasite, or something the parasite is doing to the host cell, or a combination of both? There could be a lot of things happening.”
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