Initiation of inflammation and the first line of defense
Mediator-producing cells already present in the tissue (resident cells) react to damage first: macrophages, labrocytes (mast cells), eosinophils, and natural killer (NK) cells. They trigger the vascular reaction.
Following this, polymorphonuclear leukocytes (predominantly neutrophils) massively migrate from the microvasculature into the focus. These are the "on-duty" cells of nonspecific resistance. They are the first to contact the pathogen, block its entry into the body, and destroy it via phagocytosis and exocytosis. Neutrophils provide the primary defense (especially in purulent infections), but inevitably perish in the process of carrying out their functions.
Macrophages as conductors of inflammation
The macrophage is a key cell linking the local inflammatory focus with systemic reactions of the entire organism. Contrary to common misconceptions, direct destruction of bacteria is not their main task (the bactericidal activity of macrophages is weaker than that of neutrophils).
Their main function is antigen presentation. They phagocytose damaging factors, identify antigenic determinants, and transmit this information to the immune system to trigger a specific defense.
In addition, macrophages perform a number of crucial tasks:
- Contain about 100 biologically active substances.
- Release interleukin-1 and tumor necrosis factor alpha, stimulating the formation of granulocytes in the bone marrow.
- Regulate inflammation through the activation of acute-phase reactants.
- Produce growth factors and stimulate angiogenesis for subsequent repair.
Spatial distribution within the focus
At the height of the exudative reaction, the center of the focus is oversaturated with dead leukocytes and aggressive hydrolytic enzymes. If macrophages were to head to the center, they would perish uselessly due to the high aggressiveness of the environment.
Therefore, they concentrate at the periphery, forming a cellular wall—the "second barrier." This ensures demarcation (isolation) of the inflamed zone from healthy tissues. The outcome directly depends on macrophage activity: their activation leads to the rapid formation of a robust connective tissue capsule, while their suppression leads to an increase in the zone of necrosis and suppuration.
Cellular cooperation
Macrophages actively interact with other participants in inflammation:
- With lymphocytes: This is prominently manifested in delayed-type hypersensitivity (DTH). The result can be complete immune cytolysis of the pathogen or granulomatosis. For example, in tuberculosis, incomplete phagocytosis occurs: mycobacteria are isolated inside epithelioid cells, which provides the body with non-sterile immunity and prevents the generalization of infection.
- With fibroblasts: In the repair phase, monocytes affect cells that synthesize collagen and elastin, triggering fibrillogenesis processes.
Briefly: answers to topical questions
What inflammatory mediators do mast cells (labrocytes) secrete?
Mast cells (labrocytes) release primary and secondary inflammatory mediators upon degranulation. The main ones include:
- Histamine — a biogenic amine causing mucosal edema, hypersecretion of mucus, and smooth muscle spasm.
- Leukotrienes — a complex forming the slow-reacting substance of anaphylaxis.
- Chemotactic factors — eosinophil and neutrophil factors that attract inflammatory cells to the focus.
What cells form the tuberculous granuloma?
The tuberculous granuloma is epithelioid-cellular and is formed by several types of cells arranged in layers around the central zone of caseous necrosis. Its cellular composition includes:
- Epithelioid cells — surround the zone of necrosis like a palisade.
- Pirogov–Langhans giant cells — located between epithelioid and lymphoid cells.
- Macrophages and sensitized T-lymphocytes — form a cellular wall at the periphery.
- Fibroblasts — form the outer border of the granuloma.
What enzymes are contained in neutrophil granules?
Neutrophil granules contain aggressive hydrolytic enzymes involved in the destruction of microorganisms and tissue damage. These include:
- Proteinase 3 — localized in the primary (azurophilic) granules of neutrophils.
- Myeloperoxidase — an enzyme of azurophilic granules that generates strong oxidizing agents upon interaction with hydrogen peroxide.
- Lysosomal hydrolases and proteases — released during exocytosis and phagocytosis, causing barrier destruction and tissue alteration.
What specific growth factors do macrophages produce in the repair phase?
In the repair phase, macrophages produce a number of growth factors that stimulate cell proliferation and angiogenesis. These include:
- Fibroblast growth factor — stimulates the proliferation of fibroblasts, endothelium, and smooth muscle cells.
- Epidermal growth factor — participates in cell proliferation processes.
- Transforming growth factor alpha (TGF-α) — ensures cell proliferation directly within granulation tissue.
- Transforming growth factor (TGF) — secreted by macrophages along with other cytokines.
To remember the roles of the main cells, imagine a fortress siege: Neutrophils are the infantry (going into battle first, killing the enemy, and dying en masse). Macrophages are the commanders and scouts (standing at the periphery, studying enemy antigens, calling for reinforcements, and directing wall restoration).
Class and exam questions
Who arrives first at the site of inflammation?
Local (resident) tissue cells react first, while neutrophils are the first to migrate from the bloodstream, providing early defense and blocking the pathogen.
Why do macrophages accumulate at the edges of the focus rather than in the center?
In the center of the focus, the concentration of aggressive hydrolytic enzymes and dead leukocytes is high. Macrophages would simply die there, so they form a protective demarcation wall at the periphery.
What is the significance of incomplete phagocytosis using tuberculosis as an example?
In tuberculosis, mycobacteria are not completely destroyed, but persist inside macrophages (epithelioid cells). This isolates the pathogen, prevents its spread throughout the body, and provides non-sterile immunity.
What else to study on this topic
- The effect of macrophage activity on the timing of connective tissue capsule formation.
- Mechanisms of antigen presentation and initiation of specific immunity.
- The role of interleukin-1 and tumor necrosis factor in systemic reactions of the organism.
- Delayed-type hypersensitivity: immune cytolysis and granulomatosis.
- Synthesis of collagen and elastin in the reparative phase of inflammation.
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