Introduction ============ The main reason for the occurrence of a pathological process in a tissue is the formation of its necrotic focus, that is, of the lesion containing the dead cells. The necrotic focus appears either as the result of natural causes or is a result of trauma. If there is no treatment of this focus, the pathological process spreads to the adjacent tissues, and the lesion turns into an abscess. Most frequently this happens after trauma, in cases of necrosis of tissues after trauma, in cases of severe thermal, mechanical or electrical injuries. In the case of an untreated wound and the subsequent necrosis of tissues, the latter becomes an abscess. In this case, there are four different stages of the process, beginning with the tissue necrosis, ending with the abscess ([@B1]). The process of infection spreading consists of numerous stages. The first of them is a stage of tissue necrosis, when the wound is open and the tissue is contaminated by pathogens ([@B2]). The role of this step in the inflammatory process is important. It is necessary to make the distinction between primary necrosis and secondary necrosis, both of which are important for the understanding of the mechanism of formation of an abscess. The first variant of necrosis can be a result of an infection (e.g. by necrotizing fasciitis). The latter one occurs if there was, for example, a trauma and due to its healing the necrotic focus appears, but there was no infection in the initial wound. In both cases the initial step in the development of an abscess is the necrosis of tissues and, thus, their mechanical break. If there is an infection, it is transmitted mechanically from cell to cell by means of direct contact with viable tissue or through phagocytosis. In other cases, it is necessary to use other physical factors for its transfer, for example, aerosol or even electromagnetic waves. The results of our experiments conducted in the 1980s show that microwave radiation can cause necrosis of tissues ([@B3]). The subsequent stages of infection spreading are defined according to the severity of the pathological process in the tissues. The second step in the process is a transition from necrosis to an active stage of infection, in which the microorganisms multiply in a living or dead tissue. It is during this stage that the process of necrosis and inflammation are combined, and the intensity of their interaction can determine the severity of the infection. The most likely cause of this stage is the dissemination of the pathogens from the necrotic focus, for example, through lymphatic vessels. When the second phase of infection begins, two main types of tissues can be distinguished: those with a sufficient blood supply and those with poor blood supply (hypoperfused tissue) ([@B4]). If the vascular system of the tissues is intact, the infection proceeds as in the case of a well-vascularized tissue. In the infection caused by anaerobic strains, however, the process proceeds at a slower rate. If blood circulation is poor, because of vascular insufficiency, the course of infection begins with the accumulation of pus in the necrotic focus, that is, with necrotizing fasciitis. The cells of dead cells are necrotic due to the intracellular accumulation of lactic acid and a decrease in pH values. Necrotic cells are characterized by an increase in the concentration of lactic acid and a decrease in the concentration of bicarbonates in the cell environment. In the absence of oxygen, bacteria can oxidize lactic acid, which leads to an increase in the pH value in the cell environment. This leads to a decrease in the availability of lactic acid for bacteria, which limits bacterial growth ([@B5]). The next stage is the phase of decomposition of necrotic tissue. During this phase, necrosis is transformed into a process of liquefaction and liquefied tissue is infiltrated by polymorphonuclear leucocytes (PMNs), monocytes, macrophages and lymphocytes. As a result, the infection spreads throughout the entire body, and inflammation spreads from the lesion to the adjacent tissues. Necrosis and inflammation coexist during this stage, so the inflammatory reaction and the necrotic process are closely related. The inflammatory process continues due to the action of a variety of chemotactic and nonspecific chemical factors, primarily cytokines and inflammatory mediators. In the case of trauma, the inflammatory process is particularly intense and rapidly progresses because tissue necrosis is caused not only by a microbiological factor but also by a mechanical one. The next phase in the process of infection spreading is the infection. After the death of a tissue, the bacteria grow in the liquefied tissue, forming colonies. As soon as the pathogenic bacteria penetrate the bloodstream, they reach all parts of the organism, causing septicopyemia (bacterial localization in blood and tissues). The clinical picture of septicopyemia is similar to the course of severe systemic infections with high mortality (e.g. septic shock), although septicopyemia, due to its infectious nature, is less developed. The mechanism of inflammation can be described in two stages: the stage of rapid cell proliferation with a high level of oxygen consumption, and the stage of slow cell proliferation, with a high level of lactic acid synthesis. For example, in rats, the latter stage is shorter than the stage of short-lived cells ([@B6]). It is especially important to distinguish between inflammation and necrosis, when studying wound infection ([@B7]). First, there is a direct relationship between the level of local oxygen and the production of lactic acid. Due to the decrease in the level of oxygen in the cells, lactic acid increases, which leads to hypoxia and cell necrosis. At the same time, it was also noticed that an initial stage of infection spreading has an anti-inflammatory character. The inflammatory process is limited to the surrounding tissues. These factors characterize the interaction between inflammation and necrosis ([@B7]). However, necrosis should be studied not only separately but also as a part of the inflammatory process. For example, the mechanism of infection spreading in the cells of a necrotic focus is connected with the activity of the enzymes from the mitochondrial membrane. In the case of necrosis, the mitochondrial membranes are damaged and the cell membranes are permeable. As a result, enzymes from the cytoplasm enter the cell, and the enzymes from cytoplasmic membranes are exposed to the environment ([@B8]). This is a very important observation from the viewpoint of infection spreading. It is known that cytoplasmic enzymes and extracellular enzymes differ in their affinity to antimicrobial agents ([@B9]). If inflammation and necrosis occur together, what determines the level of their influence on the body and which of them is responsible for this influence? Which components determine the severity of inflammation, necrosis and infection? There are several theories on the role of different types of cells in the mechanism of bacterial infection spreading. There is a traditional opinion that only leukocytes of the myeloid line, for example, macrophages, play an important role in the process of infection spreading. Many researchers do not agree with this opinion. According to them, the entire range of innate immunity mechanisms and effector cells is responsible for the process of infection spreading ([@B10]). The immune response begins with the recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs), mainly by Toll-like receptors (TLRs). The cells express pathogen recognition receptors (PRRs) that recognize pathogen-associated molecular patterns (PAMPs) and pathogen-specific antigens. The activation of intracellular signalling pathways in response to specific pathogenic stimuli results in the expression and release of cytokines, chemokines, and interferons, which are necessary for the effective host defense ([@B11]). According to the studies of Eberl *et al.*, the ability of leukocytes to kill bacteria depends on the presence of specific receptors that are located on their surface ([@B12]). It is not clear what are the main receptors on the surface of immune cells that contribute to the killing of bacteria in an abscess. It is known that PMNs kill bacteria with the help of extracellular traps, consisting of a web of DNA fibers that capture and kill extracellular microorganisms. The activity of PMNs and other phagocytes is not always sufficient to clear pathogens from necrotic tissue ([@B13]). Bacteria have developed different mechanisms for their own defense against the host cells. One of the methods of suppressing the oxidative burst of immune cells is the reduction of the expression of complement C3 on the surface of bacterial cells, which leads to the suppression of PMN-dependent activation ([@B14]). The virulence of bacteria depends on many factors, such as the presence or absence of capsule, the presence of various toxins and hemolysins, and different mechanisms of resistance to the action of phagocytosis. Bacteria are capable of influencing the course of an immune response either through direct interaction with immune cells or as a result of the production of certain bacterial factors that contribute to their destruction and activation ([@B14]). Bacterial toxins can induce apoptosis of immune cells, so that they are not able to respond to an infection. The bacteria have developed several mechanisms to reduce the immune response and induce cell death. For example, some proteins produced by bacteria such as α-hemolysin, hemolysin-related protein A (HlyA), and CAMP factor (Caulobacterales leukotoxin) ([@B15]). The bacteria can also destroy the functions of immune cells by means of the production of some proteases, such as staphylokinase, streptokinase and various proteases produced by gram-negative bacteria ([@B16]). The bacteria can control and regulate the immune response to prevent the body from unnecessary damage. However, they are also capable of using cellular debris to their advantage. Bacterial cells can survive for long periods of time in macrophages as a result of the production of bacterial factors that inhibit inflammation. During this period, macrophages synthesize reactive oxygen and nitrogen