Incell biology,lamellar bodies (otherwise known aslamellar granules,membrane-coating granules (MCGs),keratinosomes orOdland bodies) are secretoryorganelles found intype II alveolar cells in thelungs, and inkeratinocytes in theskin. They are oblong structures, appearing about 300-400 nm in width and 100-150 nm in length intransmission electron microscopy images. Lamellar bodies in thealveoli of the lungs fuse with thecell membrane and releasepulmonary surfactant into the extracellular space.[1][2]
Inalveolar cells thephosphatidylcholines (choline-basedphospholipids) that are stored in the lamellar bodies serve aspulmonary surfactant after beingreleased from the cell. In 1964, using transmission electron microscopy, which at that time was a relatively new tool for ultrastructural elucidation, John Balis identified the presence of lamellar bodies in type II alveolar cells, and further noted that upon theirexocytotic migration to the alveolar surface, lamellar contents would uniformly unravel and spread along the circumference of thealveolus, thus loweringsurface tension and similarly, the required alveolar inflation force.[3]
In the upperstratum spinosum andstratum granulosum layers of theepidermis, lamellar bodies are secreted fromkeratinocytes, resulting in the formation of an impermeable, lipid-containing membrane that serves as a water barrier and is required for correctskin barrier function. These bodies release components that are required for skin shedding (desquamation) in the uppermost epidermal layer, thestratum corneum.[4] These components includelipids (e.g.glucosylceramides), hydrolyticenzymes (e.g.proteases,acid phosphatases,glucosidases,lipases) andproteins (e.g.corneodesmosin).[5] Lamellar bodies have been observed to contain distinct aggregates of the secreted components glucosylceramide,cathepsin D,KLK7,KLK8 and corneodesmosin. Transportation of molecules via lamellar bodies is thought to prevent enzymes from interacting with their relevantsubstrates orinhibitors prior to secretion.[5]
Recent work suggests that lamellar bodies form a continuous membranous structure with thetrans-Golgi network.
Lamellar body secretion and lipid structure is abnormal in the epidermis of patients withNetherton syndrome, a skin disorder characterised bychronic inflammation and universalpruritus (itch).
Deficient lipid membrane causes cold damage in patients of asteatotic eczema (also known as winter eczema).[6]