The source of pain is bacteria
Last reviewed: 16.10.2021
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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 triggered, with the formation of immune cells in the affected tissues. The result is always the same - swelling, suppuration and pain. Hence toothache with caries and pain in the abdomen, as a result of intestinal infection, can be called a side effect in the work of immunity.
Sensational discovery was made by researchers from the United States. As it turned out, bacteria are able to independently activate neurons of pain. Initial interest was concerned with the interaction of neurons and immune cells upon infection. Neuronal reaction to pathogenic bacteria occurred without the participation of the immune system.
The following experiment allowed the scientists to make a comparative analysis of the number of bacteria in the code of mice infected with Staphylococcus aureus in comparison with the size of edema of the inflammatory 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 morbidity rate was recorded before the puffiness spread as much as possible.
These studies were published in the journal Nature, with information that bacteria have two kinds of substances that affect pain receptors. First of all, these are peptides of N-formylated type, with which neurons are reported. Laboratory mice without these receptors were more likely to tolerate pain. Pore-forming toxins have also been discovered that can penetrate the cell membrane with the formation of a large pore passing the ion flow stimulating the activity of neurons.
In turn, the pain receptors are able to "communicate" with immune cells, provoking a decrease in their action. The activation of neuronal pain reduced the formation of neutrophils and monocytes in the affected area. As is known, the strength of an immune response depends on the amount of these cells. Scientists were able to identify a peptide molecule, due to which pain neurons transmitted information about the need to reduce the production of inflammatory proteins to immune cells.
It is known that antigens remain from bacteria. Getting into the blood, and then into the lymph nodes, the molecules of bacteria or their particles combine with B-cells responsible for the production of antibodies. Pain receptors cope with the immune response and in this case - nerve cells have a retarding effect on the migration of T and B cells in the lymphatic system.
Disease-causing bacteria are provocateurs of pain and with the help of this painful reaction suppress the immune response against themselves.
Pain receptors try to resist the infection, trying to protect the tissue from additional damage due to inflammation, however, bacteria have a clear advantage.
If the source of pain is bacteria, it would be nice to invent a medical product that can suppress the response of pain receptors to signals from bacteria that relieve pain and simultaneously accelerate the functioning of the immune system.