New research, published in The Journal of Immunology, has found that a parasitic worm can suppress neurons in the skin to avoid detection by the host.
This adaptation likely evolved to enhance the worm’s survival, and identifying the molecules responsible could lead to the development of new painkillers.
Schistosomiasis is a parasitic infection caused by helminths, a type of worm. Infection occurs when larvae penetrate the skin during contact with contaminated water through activities like swimming, washing clothes, or fishing. Unlike many other pathogens that trigger pain, itching, or rashes, the schistosome worm often evades the immune system.
Researchers from Tulane School of Medicine investigated why the parasitic worm Schistosoma mansoni does not cause pain or itching during skin penetration.
They discovered that S. mansoni reduces the activity of TRPV1+, a protein involved in sending heat, pain, and itch signals to the brain. TRPV1+ plays a role in pain-sensing in sensory neurons and regulates immune responses in various conditions, including infections, allergies, cancer, autoimmunity, and hair growth.
The study revealed that S. mansoni produces molecules that suppress TRPV1+, blocking signals to the brain and enabling the worm to infect the skin largely unnoticed. This mechanism likely evolved to improve the worm’s chances of survival.
“If we identify and isolate the molecules used by helminths to block TRPV1+ activation, it may present a novel alternative to current opioid-based treatments for pain,” said Dr. De’Broski R. Herbert, Professor of Immunology at Tulane School of Medicine and lead author. “These molecules could also become therapeutics for reducing pain in inflammatory conditions.”
The researchers also found that TRPV1+ is essential for initiating immune protection against S. mansoni. When activated, TRPV1+ triggers a rapid mobilization of immune cells such as γδ T cells, monocytes, and neutrophils, which cause inflammation that helps resist larval entry into the skin.
This underscores the importance of pain- and itch-sensing neurons in immune defense.
Dr. Herbert suggested that identifying the molecules in S. mansoni that block TRPV1+ could pave the way for preventive treatments for schistosomiasis. “We envision a topical agent that activates TRPV1+ to prevent infection for those at risk from contaminated water,” he said.
The study involved infecting mice with S. mansoni and examining their pain sensitivity and the role of TRPV1+ in infection prevention.
The next steps include identifying the worm’s secreted or surface molecules that inhibit TRPV1+ activity and pinpointing the γδ T cell subsets responsible for immune defense, as well as exploring the broader neuronal suppression strategies evolved by helminths.
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The study is published in The Journal of Immunology.
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