Posted on 08/14/2025 11:11:41 AM PDT by Red Badger
A pair of Schistosoma mansoni seen in SEM imaging (Credit: USUHS/Public Domain)
==================================================================================
Usually, when parasitic worms attempt to invade the human body, the skin serves as the first line of defense. Pain receptors sound the alarm, prompting immune cells to swarm and stop the would-be invader in its tracks.
However, new research has discovered that one of the world’s most pervasive parasitic worms, Schistosoma mansoni, sidesteps this natural alarm system by manipulating pain-sensing neurons to infiltrate a host’s body.
A study published in The Journal of Immunology reveals how this blood fluke exploits a specialized class of neurons marked by the TRPV1 ion channel—best known for sensing heat and the burning sensation of chili peppers—to silently penetrate skin tissue, thereby avoiding detection and establishing a long-term infection.
“This work suggests that S. mansoni may have evolved to manipulate TRPV1+ neuron activation as a countermeasure to limit IL-17-mediated inflammation, facilitating systemic dissemination and chronic parasitism,” researchers write.
These findings not only provide a deeper understanding of why initial infections by S. mansoni are typically painless, unlike bacterial or fungal infections, but also open up new avenues for treatments that utilize the nervous system to activate immune defenses, offering hope for more effective management of parasitic diseases.
A Silent Parasitic Invader with Global Reach Schistosoma mansoni is a parasitic flatworm that infects over 250 million people worldwide, primarily in regions of Africa, South America, and the Middle East. Infection begins when the parasite’s larval form, called cercariae, burrows through the skin after contact with contaminated freshwater.
Unlike its avian relatives, which trigger intense itching in a condition known as swimmer’s itch, S. mansoni often slips into the body unnoticed, leading to chronic infections that can persist for years and damage vital organs.
While earlier studies have examined how the parasite evades immune detection, this new research is the first to demonstrate that S. mansoni actively suppresses TRPV1+ sensory neurons—effectively hijacking the nervous system to silence pain and immune responses at the point of entry.
Neuronal Sabotage: Turning Off the Pain
In a series of experiments, researchers infected mice with S. mansoni larvae. They then measured their response to heat using a standard thermal pain test, known as the Hargreaves assay, a widely accepted method for assessing pain sensitivity in animal models. They found that infected mice had significantly reduced sensitivity to heat in the exposed area—evidence that their TRPV1+ neurons were impaired.
To find out why, the researchers isolated sensory neurons from the infected mice. They stimulated them with capsaicin, the same compound that causes chili peppers to burn.
Typically, capsaicin triggers a spike in calcium influx and the release of neuropeptides, such as CGRP and Substance P, both of which are critical for immune signaling and inflammation. However, neurons from infected mice showed dramatically reduced responses, despite maintaining normal TRPV1 protein levels.
When neurons from healthy mice were exposed in vitro to S. mansoni antigens, they exhibited the same suppression. This suggests that the parasite secretes molecules specifically designed to deactivate TRPV1+ neurons and prevent pain-based immune activation.
To determine whether activating these suppressed neurons could fight off infection, the team turned to optogenetics. This technique uses light to control genetically modified neurons.
They engineered mice with light-sensitive TRPV1+ neurons and stimulated them with blue light before exposing them to the parasite. Remarkably, this activation significantly increased skin inflammation, boosted immune cell recruitment, and reduced the number of larvae that successfully migrated from the skin to the lungs.
“Remarkably, blue light-exposed TRPV1- ChR2 mice had significantly lower penetrating cercariae and lung larvae when compared to littermate controls,” researchers noted. “These results suggest that transdermal TRPV1þneuron activation prevented S. mansoni skin entry and dissemination by inducing neurogenic inflammation.”
This immune response was driven in large part by IL-17-producing γδ T cells—a type of immune cell primed to respond rapidly to skin invasion. These cells play a crucial role in the immune response, proliferating in response to TRPV1+ neuron activation, along with monocytes and neutrophils that secrete inducible nitric oxide synthase (iNOS), a key enzyme in killing parasites.
To test the reverse—what happens when TRPV1+ neurons are shut down—the team chemically ablated them using a potent neurotoxin called resiniferatoxin. The result: mice became far more susceptible to infection, showing higher parasite counts in the lungs and significantly weaker immune responses at the skin.
This dual approach—turning TRPV1+ neurons on and off—provided compelling evidence that these pain-sensing nerve fibers are not only critical to detecting infection but also actively drive protective immune responses when functioning correctly.
“TRPV1 neurons were both necessary and sufficient to promote cutaneous resistance against S. mansoni, primarily through inhibiting parasite dissemination to the lung,” the authors write.
The findings contribute to a growing body of research that reveals the nervous system does more than transmit pain—it plays a frontline role in detecting pathogens and coordinating immune responses.
In recent years, TRPV1+ neurons have been implicated in defending against bacterial, fungal, and allergic skin threats. However, their role varies depending on the specific context.
In some infections, TRPV1 activation actually hinders immune defenses. For example, bacterial toxins that trigger these neurons can suppress neutrophil responses, favoring colonization. However, in the case of S. mansoni, these neurons serve as a critical defense, one that the parasite has clearly evolved to counteract.
The study also raises the possibility that other parasitic helminths, such as hookworms or Strongyloides, may use similar strategies to manipulate the host’s pain and immune signaling.
By understanding how parasites like S. mansoni interact with the nervous system, researchers aim to discover new ways to enhance the body’s natural defenses. One possibility is using capsaicin-based creams or other TRPV1 agonists to preemptively activate pain-sensing neurons at the site of potential infection.
“Identifying the molecules in S. mansoni that block TRPV1+ could inform preventive treatments for schistosomiasis,” lead author and professor of immunology at Tulane School of Medicine, Dr. De’Broski R. Herbert, said in a press release. “We envision a topical agent which activates TRPV1+ to prevent infection from contaminated water for individuals at risk of acquiring S. mansoni.”
Previous studies have shown that topical capsaicin can increase IL-17 and IL-22 levels in the skin—cytokines that enhance immune readiness. The authors suggest that similar approaches might one day be used to “harden” the skin’s defenses in high-risk areas or populations.
There’s also interest in identifying the specific molecules S. mansoni uses to silence TRPV1+ neurons. These could serve as novel targets for vaccines or therapies aimed at preventing the parasite from gaining a foothold in the first place.
Ultimately, for a parasite that can persist in the human body for decades, stealth is a matter of survival. By suppressing pain, inflammation, and immune response at the very start of infection, Schistosoma mansoni executes a sophisticated biological heist. However, thanks to this new research, scientists can now work on a way to turn the parasitic worm’s own tactics against it.
Additionally, these findings could also have significant implications for advancing pain management therapies. By uncovering how Schistosoma mansoni suppresses the key drivers of heat and inflammatory pain, scientists gain new insights into how these sensory pathways can be selectively turned off.
If the parasite’s molecular tools for silencing TRPV1+ neurons can be identified and replicated, they may serve as templates for developing next-generation analgesics that target chronic pain without the side effects associated with opioids or broad-spectrum nerve blockers.
“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 reducing pain,” Dr. Herbert explained. “The molecules that block TRPV1+ could also be developed into therapeutics that reduce disease severity for individuals suffering from painful inflammatory conditions.”
If the scientists can duplicate that chemical, pain suppression without addiction!................
What a cool finding! I would agree.
Great! Now explain how to kill it.
Will it react with ivermectin?
I’ve noticed a less arthritis using ivermectin.
I need a shower now.
Right now.
More Ivermectin too.
The scientists are just now discovering its existence...........
"WE WILL BURY YOU!!!!"
3rd world countries without sufficiently clean water for laundry drinking and bathing gain exposure to the worm.
Unlike its avian relatives,....
~~~
“avian”? Wondering which word this writer meant to use....Or do birds now attack people under water?
Other species are infectious through bird droppings and eating infected birds...........
Reminds me of this:
“The Caterpillar” is probably Night Gallery’s most famous episode; and for very good reason. Next time you have an ear ache, I defy you not to think of this episode. And of earwigs.
Posted by JKM John Kenneth Muir at January 13, 2021
Biltricide
Ivermectin
Is it any worse than ascarids, hook worms or tape worms?
It can be fatal, and can cause long lasting health problems...............
My wife heard someone on a podcast say that if you eat kimchi every day you won’t have parasites.
There is also the folk remedy of a teaspoon of pure gum spirits of turpentine (NOT the stuff you buy at the paint store, but the essential oil) with some sugar. Basically a large dose of Pine Candy. Apparently parasites hate the stuff.
Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.