The leukocytes can pass through diapersis through the pores and also through the
reticuloendothelial cells of the vessel walls. That is, even though the diameter
of the pores is much smaller than that of the cell, a small portion of this
begins to flow through the pore, momentarily shrinking so as to conform to the
diameter of the pore itself.
Once the cells have penetrated into the tissue spaces, especially the
granulocytes, and a little less the large lymphocytes and monocytes, are moved
by amoeboid movements. Some cells can move into tissues up to 40 microns per
minute; that is, in a minute they can travel a space equal to three times their
total length.
Different chemicals in the tissues induce leucocytes to move or move away. This phenomenon goes under the name of chemotaxis. The products of inflammatory tissue degeneration, especially the tissue polysaccharides, and also one of the reaction products of a complex of substances known as "complement", have the ability to promote the migration of neutrophils and monocytes to the site of inflammation. Furthermore, numerous bacterial toxins can exert chemoattractant action on leukocytes. Chemotaxis depends on the existence of a concentration gradient of the chemotactic substance. The concentration is greater in the vicinity of the source of production of the substance and, as it moves away by diffusion, it decreases according to the square of the distance. Consequently, at the cell pole farthest from the source, the concentration of the chemotactic substance is lower than at the pole of the cell facing the production site of the chemotactic substance. The increased concentration on one side of the cell causes the emission of pseudopodia to the source of the substance, while in the negative chemotaxis the opposite effect occurs.
Inflammation (or inflammation) is that set of alterations that occur in the tissues following a lesion. When this occurs due to bacteria, traumas, chemicals, heat and any other factor, the injured tissue frees histamine and other humoral substances in the surrounding fluids. This causes an increase in local blood flow and an increase in the permeability of the capillaries, whereby a large quantity of liquid and proteins passes through the tissues, including fibrinogen. The result is a local edema and the extracellular and lymphatic fluid coagulate both due to the coagulant action that the tissue exudates have on the fibrinogen. Thus a fleshy edema develops in the spaces surrounding the injured cells.
It is obvious from the previous exposition that the end result of the inflammation is to "isolate" the inflamed area from the other tissues. Here the interstitial spaces and the lymphatics are blocked by the fibrin coagulum and consequently the spraying of the inflammatory zone is considerably slowed down. Therefore, the isolation of the damaged area delays the spread of bacteria and toxin products. The intensity of the inflammatory process is usually proportional to the extent of damage to the tissue. For example, when staph infections invade tissues, they release extremely deadly toxins to the cells. The result is a rapid evolution of the inflammatory process - in fact, much faster than the multiplication and diffusion capacity of the staphylococci themselves.
Thus, staphylococcal infection is rapidly "circumscribed". On the other hand, streptococci do not cause such intense local tissue destruction and, as a consequence, the isolation process develops more slowly while, in the meantime, streptococci multiply and migrate. As a result, streptococci, compared to staphylococci (see bacteria), have a greater tendency to spread throughout the body and cause death, even if in reality the staphylococci carry on the tissues a more marked destructive activity. Recall of neutrophils in the area of inflammation. In the case of damage at the level of the tissues, there are conditions such as to induce neutrophils to move towards the injured area. Firstly, neutrophils thicken on the walls of the injured capillary, a process known as margination. Then gradually the cells pass by diapedesis into the tissue spaces. Secondly, a chemoattractant attraction of neutrophils to the injured area occurs and this depends on the presence of certain bacterial or cellular products that attract neutrophils. In this way, within a few hours from the moment in which the tissues have suffered damage, the site of the lesion is filled with neutrophils.
- Promoter factor of leukocytosis. The term neutrophilia means an abnormal increase in the number of neutrophils present in the circulating blood, while the term leukocytosis refers to an increase in the total number of leukocytes. It is believed that a substance indicated as a promoter of leukocytosis is released from most inflammatory tissues. This factor spreads in the blood and reaches the bone marrow where it performs two actions: first pro-moves, in a time ranging from a few minutes to a few hours, the release from the areas of deposit in the marrow of a large number of granulocytes, especially neutrophils, the total number of which sometimes increases up to 20,000-30,000 per cubic millimeter of blood. Secondly, in the marrow the speed of granulocyte production increases by direct action of the factor, or indirectly as a result of the emission of granulocytes by the bone marrow. Within a day or two, since the beginning of inflammation, the bone marrow becomes hyperplastic and continues to produce a large number of granulocytes for as long as the inflammatory tissues continue to produce the promoter factor of the leukocytosis. In any case it is only from the medullary deposit of leucocytes that the granulocytes come in the first day, or more, until the marrow itself has had time to become hyperplastic. Fortunately, the number of neutrophils stored in the bone marrow is about 30-40 times higher than that of neutrophils that circulate in the blood under normal conditions. This means that a large reserve is available for each emergency, which can be circulated within a few hours.
Hematology