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Micrograph showing hemosiderin-laden alveolar macrophages, as seen in a pulmonary hemorrhage. H&E stain. An alveolar macrophage, pulmonary macrophage, (or dust cell) is a type of macrophage, a professional phagocyte, found in the airways and at the level of the alveoli in the lungs, but separated from their walls. [1]
They are also called pulmonary macrophages, and dust cells. Alveolar macrophages also play a crucial role in immune responses against viral pathogens in the lungs. [25] They secrete cytokines and chemokines, which recruit and activate other immune cells, initiate type I interferon signaling, and inhibit the nuclear export of viral genomes. [25]
Smoker's macrophages are alveolar macrophages whose characteristics, including appearance, cellularity, phenotypes, immune response, and other functions, have been affected upon the exposure to cigarettes. [1] These altered immune cells are derived from several signaling pathways and are able to induce numerous respiratory diseases.
Macrophages are diffusely scattered in the connective tissue and in liver (Kupffer cells), spleen and lymph nodes (sinus histiocytes), lungs (alveolar macrophages), and central nervous system (microglia). The half-life of blood monocytes is about 1 day, whereas the life span of tissue macrophages is several months or years.
Macrophages are found in essentially all tissues, [4] where they patrol for potential pathogens by amoeboid movement. They take various forms (with various names) throughout the body (e.g., histiocytes, Kupffer cells, alveolar macrophages, microglia, and others), but all are part of the mononuclear phagocyte system.
The blood–air barrier or air–blood barrier, (alveolar–capillary barrier or membrane) exists in the gas exchanging region of the lungs. It exists to prevent air bubbles from forming in the blood , and from blood entering the alveoli .
In adults, the most common cause of PAP is an autoimmunity to granulocyte-macrophage colony stimulating factor (GM-CSF), a critical factor in development of alveolar macrophages. Decreased bioavailability of GM-CSF results in poor alveolar macrophages development and function, which results in accumulation of surfactant and related products. [3]
The alveolar type II epithelial cells are more resistant to damage, so after an insult to the alveoli, most of the damage will occur to the alveolar type I epithelial cells. [5] Left side demonstrate the structure of a normal alveolus including the difference between type I and type II alveolar epithelial cells.