Blocking inflammation can lead to chronic pain

Resume: Anti-inflammatories can relieve pain in the short term, but blocking inflammation can lead to chronic pain in the long term, a new study reports.

Source: McGill University

The use of anti-inflammatory drugs and steroids to relieve pain could increase the chances of developing chronic pain, according to researchers at McGill University and colleagues in Italy.

His research calls into question the conventional practices used to relieve pain. Normal recovery from a painful injury involves inflammation, and blocking that inflammation with medication could make pain more difficult to treat.

“For many decades it has been standard medical practice to treat pain with anti-inflammatory medications. But we found that this short-term fix could lead to longer-term problems,” says Jeffrey Mogil, professor in the Department of Psychology at McGill University and chair of the EP Taylor Chair in Pain Studies.

The difference between people who improve and those who don’t

In the study published in Science Translational Medicine, the researchers examined the mechanisms of pain in both humans and mice. They found that neutrophils, a type of white blood cell that helps the body fight infection, play a key role in resolving pain.

“By analyzing the genes of people with low back pain, we saw active changes in the genes over time in people whose pain disappeared. Changes in blood cells and their activity seemed to be the most important factor, especially in cells called neutrophils,” says Luda Diatchenko, professor in the Faculty of Medicine, Faculty of Dentistry and Canada Excellence Research Chair in Pain Genetics. Human.

Inflammation plays a key role in pain resolution

“Neutrophils dominate the early stages of inflammation and set the stage for tissue damage repair. Inflammation happens for a reason, and it seems dangerous to interfere with it,” says Professor Mogil, who is also a fellow at the Alan Edwards Center for Pain Research alongside Professor Diatchenko.

Experimental neutrophil blockade in mice prolonged pain up to ten times the normal duration. Pain treatment with anti-inflammatory drugs and steroids such as dexamethasone and diclofenac also produced the same result, although they were effective against pain early on.

Pain treatment with anti-inflammatory drugs and steroids such as dexamethasone and diclofenac also produced the same result, although they were effective against pain early on. The image is in the public domain

These findings are also supported by a separate analysis of 500,000 people in the UK which showed that those taking anti-inflammatory drugs to treat pain were more likely to have pain two to 10 years later, an effect that was not seen in people taking paracetamol or antidepressants

Reconsideration of the standard medical treatment of acute pain

“Our findings suggest that it may be time to reconsider how we treat acute pain. Fortunately, pain can be eliminated in other ways that do not involve interfering with inflammation,” says Massimo Allegri, a physician at the Monza Hospital Polyclinic in Italy and the Ensemble Hospitalier de la Cote in Switzerland.

“We found that pain resolution is actually an active biological process,” says Professor Diatchenko. These findings should be followed up by clinical trials directly comparing anti-inflammatory drugs with other pain relievers that relieve aches and pains but do not disrupt inflammation.”

“The acute inflammatory response through neutrophil activation protects against the development of chronic pain” by Marc Parisien et al. was published in Science Translational Medicine.

About this pain research news

Author: press office
Source: McGill University
Contact: Press Office – McGill University
Image: The image is in the public domain.

original research: Open access.
“The acute inflammatory response through neutrophil activation protects against the development of chronic pain” by Marc Parisien et al. Science Translational Medicine


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This is a diagram of the study.

Acute inflammatory response through neutrophil activation protects against the development of chronic pain

The transition from acute to chronic pain is vitally important, but not well understood.

Here, we investigated the pathophysiological mechanisms underlying the transition from acute to chronic low back pain (LBP) and performed a transcriptome-wide analysis in peripheral immune cells from 98 participants with acute low back pain, followed for 3 months.

Transcriptomic changes were compared between patients whose low back pain resolved at 3 months with those whose low back pain persisted. We found thousands of dynamic transcriptional changes over 3 months in low back pain participants with resolved pain, but none in those with persistent pain.

Transient neutrophil-driven upregulation of inflammatory responses was protective against the transition to chronic pain. In mouse pain trials, early treatment with a steroidal or nonsteroidal anti-inflammatory drug (NSAID) also caused prolonged pain despite being a short-term analgesic; such prolongation was not observed with other analgesics.

Neutrophil depletion delayed pain resolution in mice, whereas peripheral injection of neutrophils themselves, or S100A8/A9 proteins normally released by neutrophils, prevented the development of long-lasting pain induced by an anti-inflammatory drug.

Analysis of pain trajectories from human subjects reporting acute back pain to the UK Biobank identified an elevated risk of pain persistence for subjects taking NSAIDs.

Thus, despite early analgesic efficacy, management of acute inflammation may be counterproductive to long-term outcomes for patients with low back pain.

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