When an infection appears in the body, the first to meet it are neutrophils, a class of leukocytes that are part of the innate immunity system. There are a lot of neutrophils, 50–70% of all immune cells; an adult produces about 100 billion of them every day. Neutrophils instantly sense pathogens and are the first to find themselves where the disease damages tissue. At the same time, a lot of them gather there: the first neutrophil, who senses something amiss, releases signaling molecules that attract other neutrophils – and they, in turn, immediately release the same signaling molecules, so that a huge number of cells quickly learn about the problem.
At the same time, neutrophils secrete substances directed against infection, and how inflammation develops depends largely on neutrophils. But inflammation, as you know, strikes not only bacteria and viruses, but also healthy tissues; for example, the substances with which neutrophils try to kill an infection destroy the protein and carbohydrate network that serves as the structural support for tissues. If a lot of neutrophils flock to the site of inflammation, they will become a bigger problem than the disease itself. There must be a mechanism that would prevent them from overcrowding.
Until now, it was believed that the surrounding tissue sends a signal to neutrophils that it is time for them to moderate their efforts. However, as they write in Science employees of the Institute of Immunobiology and Epigenetics Max Planck Society, neutrophils know how to do without outside advice. The very substances that they secrete and with which they call their comrades for help are then stopped. That is, the same signal can work in the opposite way: if the concentration of signaling substances does not exceed a certain limit, neutrophils move to where they are called, if the concentration becomes too high, neutrophils stop. Thus, the group of cells that deal with the infection remains not very numerous, and does not greatly harm the surrounding tissues.
But, perhaps, for the early extermination of the disease, it would be necessary to deprive the neutrophils of a sense of proportion – let there be a lot of them, let them damage healthy cells, but the infection will quickly disappear? The researchers set up an experiment in which they literally turned off the brakes of neutrophils: they stopped responding to too much signal concentration and formed a very large crowd where there were bacteria. However, there was no gain in this: a lot of neutrophils coped with bacteria no more efficiently than a smaller group of cells in which the molecular signaling brake worked. Obviously, when there are too many neutrophils, they begin to interfere with each other. Perhaps, by manipulating the ability of neutrophils to feel each other, it is possible to regulate the strength of inflammation, and weaken it when it becomes dangerous for the patient.
Source: Автономная некоммерческая организация "Редакция журнала «Наука и жизнь»" by www.nkj.ru.
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