Inflammation: the response of macrophages and granulocytes

2021-05-08 12:16 AM

Macrophages are capable of phagocytosis with more bacteria (about 5 times) and larger particles, including granulocytes. Macrophages also play an important role in initiating antibody production.

Tissue macrophages provide the first line of defence against bacterial infections

Within a few minutes of the onset of inflammation, the macrophage is ready to be present in the tissue, whether it be tissue in subcutaneous tissue, alveolar macrophages in the lungs, cerebral glioblasts, or macrophages. the other, all of which immediately begin the phagocytic activity. When activated by inflammatory and infectious products, the first effect is that the macrophages rapidly swell. The multiple macrophages then separate from the attachment site and begin to move, forming a protective barrier against infection during the first hour. The first number of macrophages mobilized is not much, but they are essential.

Neutrophils enter the inflammatory region to create a second protective barrier

During the first hour or after inflammation begins, a large number of neutrophils begin to flow into the inflamed area from the blood. This invasion is due to inflammatory cytokines (e.g., tumour necrosis factor and interleukin-1) and other biochemical products produced by the following inflammatory tissue react:

They increase the appearance of adhesion molecules, such as selectin and intercellular adhesion molecule-1 (ICAM-1), on the surface of capillary and venous endothelial cells. These adhesion molecules react with the integrin molecule on granulocytes to attach to the capillary walls and capillaries in the inflammatory region. This effect is called vascular adhesion.

They also loosen the adhesion between the capillary endothelial cells and the capillaries, allowing enough to expand so that the granulocytes crawl directly from the blood into the tissue space by the transaction.

They induce neutrophilic granulocyte kinetics toward the damaged tissue, as discussed in the previous section.

Figure. Movement of neutrophils by diapedesis through capillary pores and by chemical regulation to the area of ​​damaged tissue.

Figure. Movement of neutrophils from the bloodstream into inflamed tissue. Cytokines and other biochemical products of inflamed tissue cause increased expression of selectin and intercellular-1 adhesion molecule (ICAM-1) on the surface of endothelial cells. These adhesion molecules bind to additional molecules/receptors on the neutrophils, causing it to stick to the capillary walls or venules. The neutrophils then move across the artery wall by dipping a runny nose to the site of tissue damage

An acute increase in the number of neutrophils in the blood - "Neutrophilia"

Also, in the first few hours after an acute attack, severe inflammation, the number of neutrophils in the blood sometimes increases from 4-5 times (from 4000-5000 to 15,000-25,000 leukocytes per microliter). This is called neutrophilia, which means an increase in the number of granulocytes in the blood. Neutrophilia is caused by inflammatory products entering the bloodstream, being transported to the bone marrow, and acting on neutrophilic granulocytes stored in the bone marrow moving into the circulatory bloodstream. This causes more neutrophils to travel to inflammatory tissue.

The penetration of macrophages into inflammatory tissue creates a third protective barrier

Together with granulocytes, monocytes from the bloodstream enter inflamed tissue and become macrophages. However, the number of monocytes in the blood circulating is low. In the bone marrow, fewer monocytes are stored than neutrophils. As a result, macrophage concentration in inflammatory tissue is much slower than neutrophilic granulocytes, which takes several days to take effect. Furthermore, even after penetrating inflammatory tissue, monocytes are not mature cells, it takes 8 hours or more to swell to grow larger and develop an extremely large number of lysosomes; it is only then that they reach the top of the tissue macrophage's full capacity to be phagocytic. After a few days to weeks, the macrophage will eventually progress to phagocytosis in inflammatory tissue due to the increased production of new monocytes, which will be discussed later.

As shown, macrophages can phagocytic more bacteria (about 5 times) and larger particles, including granulocytes. Macrophages also play an important role in initiating antibody production.

The bone marrow increases the production of granulocytes and leukocytes are the fourth line of defence

The fourth protective barrier is the increased production of granulocytes and monocytes by the bone marrow. This action results from the stimulation of granulocyte and mono-clone progenitor cells in the bone marrow. However, it takes 3-4 days before granulocytes and monocytes reach the stage of leaving the bone marrow. If irritation from inflammatory tissue continues, the bone marrow can continue to produce extremely large numbers of these white blood cells for months, even years, sometimes 20 to 50 times more than normal.



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