Summary: It is a long-documented phenomenon that women experience chronic pain more frequently and for longer durations than men, but the reason why has often been dismissed as subjective. New research has uncovered a biological basis for this disparity: hormone-regulated immune cells called monocytes.<\/p>\n
The study reveals that in males, high levels of testosterone activate these cells to release IL-10, a molecule that signals neurons to shut down pain. In females, these cells are less active, leading to delayed recovery and persistent pain. This discovery shifts the focus from how pain begins to why it stays, offering a potential path for non-opioid treatments that actively resolve pain.<\/p>\n
Key Facts<\/p>\n
Active Pain Resolution: Pain relief is not a passive process; it is an active immune-driven mechanism powered by monocyte-derived IL-10.The Testosterone Trigger: Higher levels of male sex hormones, like testosterone, make monocytes more efficient at producing the \u201coff-switch\u201d for pain.Delayed Recovery in Females: Because female monocytes are less active, pain lasts longer, and the body takes more time to resolve the initial neural activation.Neural-Immune Pathway: Monocytes directly communicate with pain-sensing neurons to quiet them down.New Therapeutic Avenues: By targeting this specific pathway, researchers hope to develop non-opioid therapies that \u201cboost\u201d the immune system\u2019s ability to turn off pain.<\/p>\n
Source: Michigan State University<\/p>\n
Chronic pain lasts longer for women than men, and new research suggests differences in hormone-regulated immune cells, called monocytes, may help explain why.<\/p>\n
In a new paper in\u00a0Science Immunology, researchers at Michigan State University found a subset of monocytes release a molecule to switch off pain. These cells are more active in males due to higher levels of sex hormones such as testosterone, the team found.<\/p>\n
Females, however, experienced longer-lasting pain and delayed recovery, because their monocytes were less active.\u00a0Geoffroy Laumet, MSU associate professor of physiology, and Jaewon Sim, a former graduate student in his lab, discovered the same pattern in both mouse models and human patients.<\/p>\n
These findings, funded by the National Institutes of Health and the Department of Defense, could mean those immune cells can be manipulated into producing more signals to calm pain. While a new treatment is likely decades away, Laumet hopes this research could one day help millions of people experience relief with non-opioid treatments \u2014 and ensure women\u2019s pain is taken seriously.<\/p>\n
\u201cThe difference in pain between men and women has a biological basis,\u201d Laumet said. \u201cIt\u2019s not in your head, and you\u2019re not soft. It\u2019s in your immune system.\u201d<\/p>\n
Pain results when neurons found throughout your body are activated by stimulation. Most of the time they\u2019re silent, but they become activated when you stub your toe or fall off a bike. But for those with chronic pain, the sensors may be activated with mild stimulation, or even no stimulation at all.<\/p>\n
Doctors still rely on patients rating their pain on a scale of one to 10. The problem is everyone experiences pain differently. So, when more women than men complain of long-lasting or chronic pain, the difference is often chocked up to perception or reporting.<\/p>\n
Laumet has devoted his lab to studying pain for six years. His team was researching a small pilot project when they noticed higher levels of interleukin-10, or IL-10, in males. When the second test again showed higher levels of the substance that signals to neurons to shut down pain, they realized they were onto something.<\/p>\n
\u201cThat was the turning point for me,\u201d Sim said. \u201cI feel extremely fortunate that we trusted those early, uncertain findings and chose to pursue them further.\u201d<\/p>\n
Laumet\u2019s lab dove into the research using a sophisticated technique called high-dimensional spectral flow cytometry. They learned that monocytes, long thought to be precursor cells without much of a function, play an essential and direct role in communicating with pain-sensing neurons by producing IL-10.<\/p>\n
Laumet\u2019s team found that IL-10-producing-monocytes were much more active in males than females. When they blocked male sex hormones, they received the opposite result.<\/p>\n
\u201cThis study shows that pain resolution is not a passive process,\u201d Laumet said. \u201cIt is an active, immune-driven one.\u201d<\/p>\n
Laumet\u2019s team performed at least five types of tests on mouse models to make sure what they saw wasn\u2019t an anomaly. Each time, the results were the same.<\/p>\n
That\u2019s when he reached out to Sarah Linnsteadt, a colleague at University of North Carolina at Chapel Hill who was studying the psychological outcomes of people in car accidents. Her research showed a similar pattern \u2014 men had more active IL-10-producing-monocytes and resolved pain faster.<\/p>\n
This new evidence illuminates the immune\u2013neural pain resolution pathway, shifting the thinking from how pain starts to why pain persists. The next step is to investigate how treatments could target this pathway and boost IL-10 production. These treatments could help pain resolve faster instead of just blocking pain signals.<\/p>\n
\u201cFuture researchers can build on this work,\u201d Laumet said. \u201cThis opens new avenues for non-opioid therapies aimed at preventing chronic pain before it\u2019s established.\u201d<\/p>\n
Key Questions Answered:Q: Is women\u2019s pain really different, or do they just report it more?<\/p>\n
A: This study proves the difference is biological, not just perceptual. It\u2019s in the immune system. Because of how hormones interact with immune cells, the actual mechanism for \u201cturning off\u201d pain is slower in females.<\/p>\n
Q: Can we just give women more testosterone to fix this?<\/p>\n
A: While testosterone does trigger the monocytes, the goal isn\u2019t necessarily hormone therapy. Now that we know the monocytes are the \u201cworkers,\u201d the next step is finding a way to trigger them directly or mimic the IL-10 signal they produce, regardless of a person\u2019s hormone levels.<\/p>\n
Q: Why does this discovery matter for the opioid crisis?<\/p>\n
A: Most pain meds just block the signal. This research looks at how to end the pain by helping the body resolve it naturally. It opens the door for non-opioid treatments that actually help the body finish the job of healing.<\/p>\n
Editorial Notes:This article was edited by a Neuroscience News editor.Journal paper reviewed in full.Additional context added by our staff.About this pain and neuroscience research news<\/p>\n
Author: Bethany Mauger<\/a>
Source: Michigan State University<\/a>
Contact: Bethany Mauger \u2013 Michigan State University
Image: The image is credited to Neuroscience News<\/p>\n