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The source of the pain is bacteria
Last reviewed: 01.07.2025
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Modern medicine knows the fact that the inflammatory process provokes a response of the immune system and pain syndrome. Regardless of the type of infection, a certain chain of reactions is launched with the formation of immune cells in the affected tissues. The result is always the same - swelling, suppuration and pain. So, toothache due to caries and pain in the abdomen, as a result of intestinal infection, can be called a side effect in the work of the immune system.
A sensational discovery was made by researchers from the USA. As it turned out, bacteria are capable of independently activating pain neurons. The initial interest concerned the interaction of neurons and immune cells when an infection occurs. The neural response to pathogenic bacteria arose without the participation of the immune system.
The next experiment allowed the scientists to conduct a comparative analysis of the number of bacteria in the code of mice infected with Staphylococcus aureus, in comparison with the size of the swelling of the inflammation focus by the number of immune cells and the level of pain syndrome. It was found that there is a direct relationship between the level of pain and the number of bacteria, and the highest pain index was recorded before the swelling spread to the maximum.
The study data were published in the journal Nature, with information that bacteria have two types of substances that affect pain receptors. First of all, these are N-formylated peptides, which neurons communicate with. Laboratory mice without these receptors tolerated pain more easily. Pore-forming toxins were also discovered, which are capable of penetrating the cell membrane to form a large pore that allows an ion flow to pass through, stimulating neuronal activity.
In turn, pain receptors are able to "communicate" with immune cells, causing a decrease in their action. Activation of pain neurons reduced the formation of neutrophils and monocytes in the affected area. As is known, the strength of the immune response depends on the number of these cells. Scientists were able to identify a peptide molecule, thanks to which pain neurons transmitted information about the need to reduce the production of inflammatory proteins to immune cells.
It is known that bacteria leave antigens. Getting into the blood and then into the lymph nodes, bacterial molecules or their particles combine with B-cells responsible for producing antibodies. Pain receptors cope with the immune reaction and in this case, nerve cells have an inhibitory effect on the migration of T and B-cells in the lymphatic system.
Pathogenic bacteria are the provocateurs of pain sensations and, with the help of this painful reaction, suppress the immune response against themselves.
Pain receptors try to resist infection, trying to protect tissues from additional damage as a result of inflammation, however, bacteria have a clear advantage.
If the source of pain is bacteria, it would be nice to invent a drug that can suppress the reaction of pain receptors to signals from bacteria, eliminating pain syndrome and simultaneously speeding up the immune system.