Do not rush to remove the inflammation!
Back pain is familiar to many, and many, habitually grabbing the lower back, habitually grab nimesil or diclofenac. These nonsteroidal anti-inflammatory drugs really help at the moment of exacerbation. And recently, using the example of laboratory mice, it was shown that they can play an important role in the transition of pain syndrome to a chronic form.
Lower back pain is a very common pathology and not at all as simple as it seems. There is more and more evidence that it is a manifestation of a neuroinflammatory disease that develops as a result of a complex interaction of the nervous and immune systems.
At the site of the pathological focus, immune cells – neutrophils, monocytes, T-lymphocytes – secrete special signaling molecules that mediate the process of inflammation, as well as the regulation of pain. It is believed that such activated immune cells contribute to the transition of acute pain syndrome into chronic. However, the mechanisms of this process are practically not studied.
Recently, an international team of scientists analyzed the data of 98 patients with acute lower back pain who participated in the study PainOMICs. In the immune cells of their blood, the researchers studied the transcriptome – the whole set of RNA molecules that are "read" from the gene DNA and can serve as a measure of the synthetic activity of cells. Three months later, the study was repeated on the same patients.
By this time, some subjects had lower back pain gone, but others had turned into a chronic form. It turned out that the activity indicators of more than 1.7 thousand genes changed in people from the first group. Among these genes are those associated with the development of inflammation, whose activity depends on the activation of neutrophils. But in patients with constant pain, no such changes were noted. What is the reason?
After analyzing the data of several thousand people from the UK Biobank project database, the researchers found that lower back pain became chronic 1.76 times more often when taking nonsteroidal anti-inflammatory drugs. As you know, it is these non-hormonal drugs that have a complex (antipyretic, anti-inflammatory and analgesic) effect that are often assigned the role of an ambulance in the acute phase of inflammation.
A series of experiments on mice – models of lower back pain syndrome – showed that in these animals, taking anti-inflammatory drugs (both steroid dexamethasone and nonsteroidal diclofenac) effectively reduces pain, but prolongs the painful condition and inflammation in general. Other analgesics, for example, lidocaine, did not cause such an effect.
When the researchers blocked the activation of neutrophils in mice with the help of antibodies, the duration of the pain syndrome in them increased by an order of magnitude. At the same time, the introduction of neutrophils themselves or proteins synthesized by them in the acute phase of inflammation to animals receiving anti-inflammatory therapy prevented the transition of pain into a chronic form.
It turns out a paradoxical situation. It turns out that the development of inflammation at the acute stage of pain syndrome is an adaptive process and is aimed at solving the problem that has arisen. But if we take anti-inflammatory drugs, we relieve the severity of the pain, but the problem itself remains, as a result of which the pain can become permanent.
So far, scientists do not give practical recommendations, including to those people who often suffer from back pain and already habitually drink anti-inflammatory drugs. However, the results they obtained are a good reason to think for those who have grasped a sore back for the first time.
Article by Parisien et al. Acute inflammatory response via neutrophil activation protects against the development of chronic pain is published in the journal Science Translational Medicine.
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