Goals and types of adaptive reactions
The development of an infectious process is always accompanied by the activation of the patient's defense forces. These reactions can be innate, adaptive, or manifest as allergic or autoimmune processes.
Globally, the macroorganism pursues three goals:
- To recognize the invading pathogen.
- To eliminate the pathogen and remove it from the body.
- To repair structural and functional damage caused by the disease.
Classification of defense mechanisms
To prevent the development of infection, the body uses two echelons of defense that work in close synergy, enhancing overall effectiveness:
- Nonspecific factors. This is a universal defense that is triggered upon contact with any foreign agent. These include mechanical barriers, reflex reactions, phagocytosis, white blood cell activity, and the bactericidal properties of biological fluids.
- Specific (immunogenic) factors. Aimed at combating a specific, already recognized microorganism. They include cellular and humoral immune responses.
First line of defense: barriers and secretions
Many pathogens (for example, in contact infections) can penetrate inside only if the integument is damaged. Healthy skin protects us thanks to a dense stratum corneum and continuous epithelial desquamation (shedding), which mechanically removes bacteria.
Inside the body, its own anatomical and histological barriers operate: ciliated epithelium in the bronchi, brush border in the intestine, as well as histohematic barriers (including the blood-brain barrier) and cell membranes.
The chemical properties of secretions play a huge role:
- Secretory immunoglobulins (especially IgA). They block bacterial ligands, preventing them from attaching to epithelial receptors. Clinical fact: newborns initially have low levels of secretory IgA, making them extremely vulnerable to bacterial infections.
- Lysozyme and glycoproteins (IgM).
- Low pH. Lactic acid from sweat and fatty acids on the skin, as well as hydrochloric acid in the stomach, create a lethal environment for microbes. The stomach is practically the only part of the GI tract that normally lacks live bacteria.
Role of P-glycoprotein
This is a crucial factor that prevents bacterial toxins from massively penetrating through mucous membranes. It acts as a cellular pump, expelling biological substrates from cells back into the organ lumen.
In the small intestine, it limits the absorption of toxins; in the liver and kidneys, it accelerates their excretion with bile and urine; and in barrier tissues, it blocks their inward progression. Experiments show that a genetic defect (gene knockout) of P-glycoprotein in mice dramatically increases their susceptibility to colitis.
Cellular defense and phagocytosis
If the barriers are breached, leukocytes (mononuclear and granulocytes, primarily neutrophils) come into play. They destroy the enemy directly or by releasing special substances — leukokins.
The key process here is phagocytosis. This is the engulfment and intracellular destruction of the microbe. The main phagocytic cells are:
- Blood neutrophils and monocytes.
- Tissue macrophages (alveolar macrophages in the lungs, Kupffer cells in the liver, dendritic and stellate cells).
The process proceeds in stages: first, the microbe adheres to the phagocyte (adhesion), then it is engulfed, after which a powerful microbicidal system is activated inside the cell. It is divided into oxygen-dependent and oxygen-independent subsystems, which ultimately inactivate and destroy the pathogen.
Briefly: answers to topical questions
What are the stages (phases) of phagocytosis?
The process of phagocytosis traditionally consists of eight consecutive stages.
- Chemotaxis — directional movement of the phagocyte toward the object (approach) and cell polarization.
- Adhesion — establishment of contact and attachment of the phagocyte to the object after its recognition.
- Membrane activation — preparation for engulfment.
- Immersion — wrapping around the object.
- Phagosome formation — closure of the membrane and complete engulfment.
- Phagolysosome fusion — formation of a single structure.
- Killing and digestion — intracellular destruction of the microbe.
- Release of degradation products — removal of residues from the cell.
To remember the stages of phagocytosis, use the "APA" rule: Adhesion (attachment) — Phagocytosis/Engulfment (capture) — Activation (activation of microbicidal systems and destruction).
Class and exam questions
Why does dysbiosis increase the risk of infectious diseases?
Normal microflora of the skin and mucous membranes (at the correct amount and ratio of bacteria) performs a protective function. In dysbiosis, this defense weakens, facilitating the invasion of pathogenic microbes.
How does the skin protect us from bacteria, besides acting as a mechanical barrier?
The skin exhibits pronounced bactericidal properties due to its low pH. Sweat glands secrete lactic acid, and fatty acids are present on the surface, creating unfavorable conditions for the survival of microorganisms.
What is the function of secretory IgA on mucous membranes?
It binds ligands on the bacterial surface, physically preventing their attachment (adhesion) to specific receptors on our epithelial cells.
What else to study on this topic
- Oxygen-dependent and oxygen-independent mechanisms of the phagocyte microbicidal system.
- Mechanisms of action of leukokins during the development of an infectious process.
- Cellular and humoral reactions of specific immunity.
- Pathogenesis of infections in congenital secretory IgA deficiency.
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