Phagocytic capabilities

Weiss and coworkers73 discussed evidence for the assumption that the ability of cancer cells to grow in the host revealed the failure of antibody formation or of phagocytic capability of the reticuloendothelial system. 

White cells are physiologically and pathologically important as mediators of the inflammatory response (reviewed in [288]). Neutrophils are the first of the inflammatory cells to arrive at sites of injury. The neutrophils phagocytic capabilities and the release of proteinases and oxidants are important for fighting bacterial infections as well as clearing dead cell... 

It has been suggested that receptors on phagocytes capable of recognizing C3 in effect cement a particle to the white cell, thereby facilitating both phenomena. There is evidence, however, that the fixation of C5 may also be required for phagocytosis of certain microorganisms, such as monilia (30). 

Dead or live bacteria may be effective to stimulate inflammatory reactions of phagocytic cells against tumor cells. The best-characterized treatment is the use of Bacillus Calmette Guerin (BCG) in the case of bladder cancer where activation of the immune response is capable of controlling tumor growth. 

The mature vitreous contains a class of mononuclear phagocytic cells called hyalocytes (Balzas and Delinger, 1984). These cells are generally embedded in the vitreous humour 20-50 /tM away from the basal lamina, forming a single layer of scattered cells. In the developing eye they are located more centrally and are capable of synthesizing the main solid constituents of the vitreous gel. 

The most notable medical application of IFN-y relates to the treatment of CGD, a rare genetic condition with a population incidence of between 1 in 250 00 and 1 in 1 000 000. Phagocytic cells of patients suffering from CGD are poorly capable/incapable of ingesting or destroying infectious agents such as bacteria or protozoa. As a result, patients suffer from repeated infections (Table 8.10), many of which can be life threatening. 

Cassatella, M. A., Bazzoni, F., Flynn, R. M., Dusi, S., Trinchieri, G., Rossi, F. (1990). Molecular basis of interferon-/ and lipopolysaccharide enhancement of phagocyte respiratory burst capability. J. Biol. Chem. 265, 20241-6. 

Tumor necrosis factor (TNF)a is capable of suppressing viral replication and also activates phagocytes. 

G-CSF activates neutrophils, transforming them into cells capable of respiratory burst and release of secretory granules. It also modulates the expression of adhesion molecules on neutrophils as well as CD1 lb/CD18 and plasma elastase antigen levels. G-CSF induces proliferation of endothelial cells, phagocytic activity of neutrophils, reactive oxygen intermediate production by neutrophils and antibody-dependent cellular toxicity by neutrophils. 

Gold alters the morphology and functional capabilities of human macrophages—possibly its major mode of action. As a result, monocyte chemotactic factor-1, interleukin-8, interleukin-IB production, and vascular endothelial growth factor are all inhibited. Intramuscular gold compounds also alter lysosomal enzyme activity, reduce histamine release from mast cells, inactivate the first component of complement, and suppress the phagocytic activities of polymorphonuclear leukocytes. Auranofin also inhibits release of prostaglandin E2 and leukotriene B4. 

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