Search results
Results from the WOW.Com Content Network
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]
Mucociliary clearance (MCC), mucociliary transport, or the mucociliary escalator describes the self-clearing mechanism of the airways in the respiratory system. [1] It is one of the two protective processes for the lungs in removing inhaled particles including pathogens before they can reach the delicate tissue of the lungs.
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]
The cells are primarily monocytes and macrophages, and they accumulate in lymph nodes and the spleen. The Kupffer cells of the liver and tissue histiocytes are also part of the MPS. The mononuclear phagocyte system and the monocyte macrophage system refer to two different entities, often mistakenly understood as one. [citation needed]
A siderophage is a hemosiderin-containing macrophage. Heart failure cells are siderophages generated in the alveoli of the lungs of people with left heart failure or chronic pulmonary edema, when the high pulmonary blood pressure causes red blood cells to pass through the vascular wall. [1] Siderophages are not specific of heart failure.
In anatomy the term reticuloendothelial system (abbreviated RES), often associated nowadays with the mononuclear phagocyte system (MPS), was employed by the beginning of the 20th century to denote a system of specialised cells that effectively clear colloidal vital stains (so called because they stain living cells) from the blood circulation ...
The short-term exposure attracts macrophages and neutrophils to the lung with a 4-fold increase in cellularity. [ 4 ] [ 2 ] Short duration also biases polarization towards M1 phenotype. The number of immune cells however will be normalized in 6 months, demonstrating the shift in signaling direction.
The activation of T H 1 and M1 macrophage is a positive feedback loop, with IFN-γ from T H 1 cells upregulating CD40 expression on macrophages; the interaction between CD40 on the macrophages and CD40L on T cells activate macrophages to secrete IL-12; and IL-12 promotes more IFN-γ secretion from T H 1 cells.