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Phagocytosis Opsonin

Compared with phagocytosis, pinocytosis appears to be a universal phenomenon in all cells, including phagocytes. Unlike phagocytosis, which is mediated by the serum opsonin, pinocytosis does not require any external stimulus. Pinocytosis is divided into two types fluid-phase pinocytosis and adsorptive pinocytosis (see Fig. 3B). Fluid-phase pinocytosis is a nonspecific, continuous process, and it is believed to be useful as a general process for transporting macromolecular constructs through epithelia, some endothelia, and into various blood cells. Adsorptive pinocytosis, in... [Pg.534]

Figure 1.4. Recognition of bacteria by neutrophils. Invading bacteria are opsonised by serum proteins, such as complement fragments (e.g. C3b) and immunoglobulins. The plasma membranes of neutrophils possess receptors for these opsonins (e.g. Fc receptors and complement receptors). Thus, occupancy of these opsonin receptors triggers phagocytosis and activates events such as the respiratory burst and degranulation. Note that the receptors and opsonins are not drawn to scale. Figure 1.4. Recognition of bacteria by neutrophils. Invading bacteria are opsonised by serum proteins, such as complement fragments (e.g. C3b) and immunoglobulins. The plasma membranes of neutrophils possess receptors for these opsonins (e.g. Fc receptors and complement receptors). Thus, occupancy of these opsonin receptors triggers phagocytosis and activates events such as the respiratory burst and degranulation. Note that the receptors and opsonins are not drawn to scale.
The precise function of many acute-phase proteins is not known. C-reactive protein binds lipids, whilst a-macroglobulin and ceruloplasmin can scavenge some reactive oxygen metabolites. However, many acute-phase proteins are glycoproteins and can bind to bacterial surfaces hence, they may serve as non-specific opsonins for phagocytosis, and their synthesis is stimulated by IL-1 and IL-6. [Pg.27]

Bacteria bind to complement components and the bacterium-complement complexes bind complement receptors on the surface of macrophages. Phagocytosis may also be mediated by specific antibodies that function as opsonins, which bind to particles, rendering them susceptible to phagocytosis. The bacterium-antibody complex then binds the macrophages via the Fc receptor and phagocytosis begins. [Pg.656]

This repulsive steric layer reduces the adsorption of opsonins and consequently slows down phagocytosis. The net effect of PEG attachment is that macrophage/liver uptake of the particles is delayed or reduced, thus increasing the circulation time.1... [Pg.111]

Cleaves to produce C3a and C3b. C3a stimulates histamine release by mast cells, thereby producing vasodilation. C3b is able to bind to bacterial cell walls and act as an opsonin, which marks the invader as a target for phagocytosis. Stimulates histamine release by mast cells, thereby producing vasodilation. It is also able to act as a chemoattractant to direct cells via chemotaxis to the site of inflammation. [Pg.215]

An opsonin is any molecnle that acts as a binding enhancer for the process of phagocytosis. [Pg.229]

Causes The following causes are seen as being responsible for an acquired immune deficiency syndrome in liver cirrhosis (B.A. Runyon, 1995) (i.) hypofunction of the RES (a decrease in the filter or clearance function and phagocytosis capacity as well as reduced formation of immune modulators) (s. p. 65), (2.) reduction in hepatic synthesis of opsonins (s. p. 66), (3.) compromised function of leucocytes, (4.) impaired proliferation and activation of T lymphocytes, and (5.) increased mucosa permeability to bacteria. Both bacteria and bacterial lipopolysaccharides enter the organism in large numbers. They are responsible for increased serum levels of the cytokines (e. g. interleukins 1 and 6, TNF, y-interferon), and there is increased production of these substances together with their reduced breakdown in the cirrhotic liver. Cytokines are formed in the monocytes of blood and in the mononuclear cells of various organs (above all in ascites). [Pg.731]

C3b (opsonin) A component of the complement system which can promote phagocytosis of the antigen-antibody complex to which it has adhered. [Pg.303]

Stossel, T. P., Quantitative studies of phagocytosis. Kinetic effects of cations and heat-labile opsonin. J. Cell Biol. 58, 340-356 (1973). [Pg.154]


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