Acinus architecture: dichotomous branching
The acinus is built on the principle of dichotomous (two-way) branching of a single terminal bronchiole. The terminal bronchiole itself does not participate in gas exchange — it is the final link of the air-conveying tract. The respiratory division begins immediately beyond it.
Branching order of acinar elements:
- Respiratory bronchioles (RB). Divided into three orders (1st, 2nd, and 3rd). Their main distinguishing feature is the presence of opening alveoli in the wall. The higher the order, the more alveoli. The epithelium here is single-layer cuboidal, with bundles of smooth myocytes persisting between the alveoli.
- Alveolar ducts. Formed by the division of 3rd-order RBs. Their wall is practically absent and consists of the openings of closely apposed alveoli. Characteristic "knob-like" thickenings are visible on histological sections — remnants of the wall with bundles of smooth myocytes and epithelium projecting into the lumen.
- Alveolar sacs. Terminal structures representing blind clusters ("bunches") of alveoli. Here, the smooth muscle "knobs" disappear completely, and the walls between alveoli become extremely thin.
Cellular composition: from bronchioles to alveoli
As one moves deeper into the acinus, the cellular landscape changes. In respiratory bronchioles, the epithelium contains ciliated, brush, and predominantly Clara cells. The latter play the role of stem elements, secrete anti-adhesive factors, detoxify xenobiotics, and prevent connective tissue proliferation.
In the alveoli themselves (gas exchange vesicles), the lining is represented by a simple squamous epithelium consisting of two cell types:
- Type 1 alveolar epithelial cells (respiratory pneumocytes). Have an extremely thin and extended anuclear part. They occupy 95% of the alveolar area and are the main component of the air-blood barrier.
- Type 2 alveolar epithelial cells (secretory pneumocytes). Large cuboidal cells occupying only 5% of the area. Contain specific osmiophilic cytophospholiposomes (lamellar bodies). Their task is the synthesis and secretion of surfactant, as well as the regeneration of the alveolar epithelium.
Surfactant complex and air-blood barrier
Gas exchange occurs across the air-blood barrier via simple diffusion. It includes: surfactant, type 1 alveolar cell, common basal membrane, and thinned capillary endothelial cell.
Surfactant is a complex of surface-active substances (90% lipids, 10% proteins) lining the alveoli. It has a two-phase structure: a liquid hypophase (molecule reservoir) and a membrane phase at the air interface.
Surfactant functions change during the respiratory cycle:
- During inspiration: molecules move from the hypophase to the surface layer. This reduces surface tension and facilitates alveolar expansion.
- During expiration: the layer thickens, and molecules return to the hypophase. The phospholipid, solid at body temperature, prevents the membrane phase from disappearing, preventing complete collapse and adhesion of the alveoli.
Clinical significance: in premature infants, due to the immaturity of type 2 alveolar cells, a surfactant deficiency occurs, leading to failure of alveolar expansion (atelectasis) and respiratory distress syndrome.
Interalveolar septum and interstitium
Adjacent alveoli are separated by interalveolar septa. They are based on loose fibrous connective tissue and a dense capillary network. To equalize air pressure between alveoli, there are through-openings in the septa — Pores of Kohn.
The cellular composition of the interstitium is specific:
- Lipofibroblasts: contact type 2 alveolar cells, accumulate lipids, and serve as substrate donors for surfactant synthesis.
- Alveolar macrophages: can migrate to the surfactant surface. They phagocytose dust, excess surfactant, and erythrocytes (during blood stasis).
- Plasmacytes and mast cells: provide local humoral immunity (antibody synthesis) and release histamine/serotonin.
The most important non-cellular component of the septa is elastic fibers. They create the elastic recoil of the lungs, causing them to collapse during expiration. When the elastic framework is destroyed (e.g., in emphysema), the alveoli remain overextended, which critically impairs gas exchange.
Briefly: answers to topical questions
What cell types form the epithelial lining of the respiratory bronchioles?
The epithelial lining of the respiratory bronchioles is formed by a single-layer cuboidal epithelium including three main cell types.
- Secretory Clara cells — most common.
- Ciliated cells.
- Brush cells.
What specific proteins are part of surfactant?
Specific proteins make up 10% of surfactant mass and are subdivided into four groups. The surfactant proteins named in sources include:
- surfactant protein A (SP-A);
- surfactant protein B (SP-B, SpB);
- surfactant protein C (SP-C, SpC);
- surfactant protein D (SP-D).
Branches of which blood vessels form the capillary network of interalveolar septa?
The capillary network of interalveolar septa and alveoli is formed by pulmonary circulation vessels. The capillary segment where gas exchange occurs is formed from branches of the pulmonary arteries originating from the pulmonary trunk.
Order of acinar structures: TRAB-AM (Terminal bronchiole → Respiratory bronchiole → Alveolar Duct → Alveolar Sac).
Class and exam questions
What mechanism prevents alveoli from collapsing during expiration?
Surfactant prevents collapse. The specific phospholipid in its composition remains solid at body temperature and is retained in the surface layer during expiration, preventing the walls from sticking together.
What are the pores of Kohn and what is their function?
These are through interalveolar openings in the septa. They are necessary to equalize air pressure between adjacent alveoli, but in pathology they can become a pathway for rapid infection spread.
Which cells produce surfactant and where are they located?
Surfactant is synthesized by type 2 alveolar cells (secretory cells). They are located on the alveolar basement membrane and contain characteristic lamellar bodies (cytophospholiposomes).
What else to study on this topic
- Metabolic function of alveolar capillary endothelium (angiotensin-converting enzyme processing and erythropoietin secretion).
- Ultrastructural organization of Clara cells and their stem cell potential.
- Immune function of surfactant: mechanisms of macrophage and lymphocyte regulation by complex proteins.
- Histogenesis and migration pathways of alveolar macrophages after phagocytosis.
- Pathomorphology of emphysema: mechanism of destruction of interstitial elastic fibers.
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