Acinus Architecture: Dichotomous Branching
The acinus is constructed 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 segment of the conducting pathway. Immediately beyond it lies the respiratory zone.
Branching order of acinar elements:
- Respiratory bronchioles. Divided into three orders (1st, 2nd, and 3rd). Their main distinguishing feature is the presence of alveoli opening into their walls. The higher the order, the more alveoli are present. The epithelium here is simple cuboidal, with bundles of smooth myocytes persisting between the alveoli.
- Alveolar ducts. Formed by the division of 3rd-order respiratory bronchioles. Their wall is practically absent and consists of the openings of closely apposed alveoli. Histological sections reveal characteristic "knob-like" thickenings—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 the respiratory bronchioles, the epithelium contains ciliated cells, brush cells, and predominant Club cells (formerly Clara cells). The latter act as stem cells, secrete anti-adhesive factors, detoxify xenobiotics, and prevent connective tissue proliferation.
In the alveoli themselves (gas exchange sacs), the lining is formed by a simple squamous epithelium consisting of two cell types:
- Type I alveolar cells (type I pneumocytes / respiratory cells). Possess an extremely thin and extended anucleate region. They occupy 95% of the alveolar area and are the primary component of the blood-air barrier.
- Type II alveolar cells (type II pneumocytes / secretory cells). Large cuboidal cells occupying only 5% of the area. They contain specific osmiophilic cytophospholiposomes (lamellar bodies). Their role is the synthesis and secretion of surfactant, as well as the regeneration of the alveolar epithelium.
Surfactant Complex and the Blood-Air Barrier
Gas exchange occurs across the blood-air barrier via simple diffusion. It includes: surfactant, a type I alveolar cell, a fused basement membrane, and a thinned capillary endothelial cell.
Surfactant is a surface-active complex (90% lipids, 10% proteins) lining the alveoli. It has a biphasic structure: a liquid hypophase (molecular reservoir) and a membrane phase at the air-liquid interface.
Surfactant functions vary throughout the respiratory cycle:
- During inspiration: molecules transition from the hypophase into the surface layer, lowering surface tension and facilitating 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, thus preventing complete alveolar collapse and atelectasis.
Clinical significance: in premature infants, immaturity of type II alveolar cells leads to a surfactant deficiency, resulting in alveolar collapse (atelectasis) and respiratory distress syndrome.
Interalveolar Septum and Interstitium
Adjacent alveoli are separated by interalveolar septa. Their core consists of loose fibrous connective tissue and a dense capillary network. To equalize air pressure between alveoli, perforations called pores of Kohn exist within the septa.
The cellular composition of the interstitium is specific:
- Lipofibroblasts: contact type II alveolar cells, store lipids, and act as substrate donors for surfactant synthesis.
- Alveolar macrophages: can migrate onto the surfactant surface, phagocytosing dust, excess surfactant, and erythrocytes (during circulatory congestion).
- Plasma cells and mast cells: provide local humoral immunity (antibody synthesis) and release histamine/serotonin.
A vital non-cellular component of the septa is elastic fibers. They generate lung recoil, causing the lungs to deflate upon expiration. When the elastic framework is destroyed (e.g., in emphysema), alveoli remain overstretched, severely impairing gas exchange.