Blocking inflammation can lead to chronic disease

Summary: Anti-inflammatory drugs can reduce pain in the short term, but blocking inflammation can lead to long-term chronic disease, according to a new study.

A source: McGill University

According to researchers at McGill University and colleagues in Italy, the use of anti-inflammatory drugs and steroids to reduce pain increases the risk of developing chronic disease.

Their research calls into question the traditional practices used to alleviate the disease. Normal recovery from an injury involves inflammation, and this inflammation can be treated with medication to make the disease more difficult to treat.

“For decades, anti-inflammatory drugs have been the standard medical practice. However, we have found that this short-term correction can lead to long-term problems, ”said Jeffrey Mogil, a professor of psychology at McGill University and chairman of the EP Taylor in pain research.

The difference between being better and being worse

In a study published in Science Translational Medicine, the researchers studied the mechanisms of the disease 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 fighting disease.

“In the analysis of the genes of people suffering from low back pain of the year, we observed that the genes of people with the disease change actively over time. Changes in blood cells and their activity have been shown to be the most important factor, especially in cells called neutrophils, ”said Luda Diatchenko, a professor at the Faculty of Medicine and the Excellence Research Chair at the Faculty of Dentistry and Canadian Human Disease Genetics.

Inflammation plays a key role in resolving the disease

“Neutrophils predominate in the early stages of inflammation and help to repair tissue damage. Inflammation can occur for any reason and it seems dangerous to intervene, ”said Professor Mogil, who is also a member of the Alan Edwards Center for Disease Research with Professor Diatchenko.

Experimental inhibition of neutrophils in mice extended the disease up to ten times longer than normal. Treatment with anti-inflammatory drugs and steroids such as dexamethasone and diclofenac gave the same results, but they were effective against the disease early.

Treatment with anti-inflammatory drugs and steroids such as dexamethasone and diclofenac gave the same results, but they were effective against the disease early. Image in public domain

These findings are confirmed by a separate analysis of 500,000 people in the UK, who have shown that those who use anti-inflammatory drugs to treat the disease are more likely to get it in two to ten years. antidepressants.

Review of standard medical treatment for severe pain

“Our results show that it is time to reconsider the treatment of acute illness. Fortunately, the disease can be killed in other ways that do not prevent inflammation, ”said Massimo Allegri, a doctor at the Monza Hospital Polyclinic in Italy and Ensemble Hospitalier de la Cote in Switzerland.

“We have found that eradication is actually an active biological process,” says Professor Diatchenko. These findings should be made after clinical trials that directly compare anti-inflammatory drugs with other pain killers that reduce pain and pain but do not stop the inflammation.

“Acute inflammatory response through neutrophil activation protects against the development of chronic disease,” Marc Parisien et al. published in Science Translational Medicine.

It’s about the disease research message

Author: Press service
A source: McGill University
The connection: Press Service – McGill University
Photo: Image in public domain

Original study: Open access.
“Acute inflammatory response through neutrophil activation protects against the development of chronic disease,” Marc Parisien et al. Science Translational Medicine


Abstract

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Acute inflammatory reaction by activating neutrophils protects against the development of chronic disease

The transition from acute to chronic disease is very important, but not well understood.

Here, we studied the acute pathophysiological mechanisms of transition from acute to chronic low back pain (LBP) and conducted a transscriptome-extensive analysis of peripheral immune cells of 98 participants with LBP, followed for 3 months.

Transcriptomic changes were compared between patients who resolved LBP at 3 months and those who retained LBP. We cured thousands of dynamic transcriptional changes in 3 months from LBP participants, but none in people with chronic disease.

Regulation of transient neutrophil-mediated inflammatory reactions has been shown to prevent the development of chronic disease. Mouse pain tests, early treatment with steroidal or non-steroidal anti-inflammatory drugs (NSAIDs) also resulted in chronic pain, despite being a short-term analgesic; Such prolongation has not been observed with other analgesics.

Decreased neutrophil counts slowed the progression of the disease in mice, and peripheral injection of neutrophils themselves or the development of long-term disease caused by the anti-inflammatory drug S100A8 / A9, usually produced by neutrophils.

Analysis of the disease trajectories of human subjects who reported severe low back pain at the UK Biobank revealed an increased risk of disease resistance for subjects receiving NSAIDs.

Thus, despite its initial analgesic efficacy, acute inflammation management may be counterproductive for long-term outcomes in LBP patients.

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