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Host Defense Mechanisms in Infection

For medical students2 min readUpdated 2026-10-10

When a pathogen invades a host organism, a cascade of adaptive reactions is triggered to detect, destroy the foreign agent, and repair damaged tissues. All defense factors are divided into two synergistic groups: nonspecific barriers that operate against any threats, and specific immunity targeted at a particular microorganism.

First lineNonspecific mechanical barriers of the skin and mucous membranes.
MicrofloraNormal biocenosis protects against pathogens, whereas dysbiosis facilitates the development of infection.
Acid barrierLow pH of gastric juice and skin is lethal to most microbes.
PhagocytosisIntracellular digestion of pathogens by macrophages and neutrophils.

Goals and Types of Adaptive Responses

The development of an infectious process is always accompanied by the activation of the patient's defense mechanisms. These reactions can be innate, adaptive, or manifest as allergic or autoimmune processes.

Globally, the macroorganism pursues three goals:

  1. To recognize the invading pathogen.
  2. To eliminate the pathogen and clear it from the body.
  3. To repair structural and functional damage caused by the disease.

Classification of Defense Mechanisms

To prevent the development of an infection, the body employs two echelons of defense that work in close synergy, enhancing overall efficacy:

First Line of Defense: Barriers and Secretions

Many pathogens (e.g., in contact infections) can penetrate inside only if epithelial integrity is compromised. Healthy skin protects us through a dense stratum corneum and continuous desquamation of the epithelium, which mechanically removes bacteria.

Inside the body, distinct anatomical and histological barriers operate: ciliated epithelium in the bronchi, the 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 massive role:

Role of P-Glycoprotein

This is a crucial factor that prevents bacterial toxins from massively penetrating mucous membranes. It functions 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 deeper penetration. Experiments show that in genetic defects (gene knockout) of P-glycoprotein in mice, susceptibility to colitis increases dramatically.

Cellular Defense and Phagocytosis

If the barriers are breached, leukocytes (mononuclear cells and granulocytes, primarily neutrophils) step in. They destroy the enemy directly or by releasing special substances known as leukokinins.

The process occurs in stages: first, the microbe adheres to the phagocyte (adhesion), then it is engulfed, after which a potent microbicidal system is activated inside the cell. It is divided into oxygen-dependent and oxygen-independent subsystems, which ultimately inactivate and destroy the pathogen.

Mnemonic

To remember the stages of phagocytosis, use the rule "APA": Adhesion (attachment) — Phagocytosis/Ingestion (capture) — Activation (activation of microbicidal systems and destruction).

Frequently asked questions

What stages (phases) does the process of phagocytosis consist of?

The process of phagocytosis traditionally consists of eight sequential stages:

  • Chemotaxis — directed movement of the phagocyte toward the object (approach) and cell polarization.
  • Adhesion — establishing 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 enclosure.
  • Phagolysosome fusion — merging of the phagosome and lysosome into a single structure.
  • Killing and digestion — intracellular destruction of the microbe.
  • Release of degradation products — removal of remnants from the cell.
Why does dysbiosis increase the risk of infectious diseases?

Normal microflora of the skin and mucous membranes (at the correct quantity and ratio of bacteria) performs a protective function. During 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 possesses pronounced bactericidal properties due to a 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 surface of bacteria, physically preventing their attachment (adhesion) to specific receptors on our epithelial cells.

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