Phagocytic cells respiratory burst

Low levels of mercuric chloride in polymorphonuclear cells may profoundly alter the cell respiratory burst, measured as chemiluminiscence, oxygen consumption and H2Oz production [171-173], depress phagocytic capacity [172, 173] and enhance release of lysosomal enzymes [ 172] with minimal loss of cell viability. A stimulation of oxygen metabolism in vivo might promote tissue injury, via the local production of free oxygen metabolites, in addition to depression of host defence [173],... 

Sometimes PD properties are common across species, thus allowing for pertinent toxicity data to be collected from a variety of species. An example of this is granulocyte colony stimulating factor (G-CSF), a cytokine produced by various cells including monocytes, fibroblasts, and endothelial cells that regulates the production of neutrophils within the bone marrow, influences neutrophil proliferation and differentiation, and contributes to increased phagocytic function, respiratory burst, and antibody-dependent killing. Keller... 

The Respiratory Burst of Phagocytic Cells Involves NADPH Oxidase Helps Kill Bacteria... 

Nitric oxide and eicosanoid synthesis haem synthesis. The importance of the pentose phosphate pathway reduced glutathione in maintaining red cell integrity. The respiratory burst in phagocytes. Clotting and complement enzyme cascades. Metabolism of lipoproteins. 

IFN-y also induces the costimulatory molecules on the macrophages, which increases cell-mediated immunity. As a consequence, there is activation and increase in the tumoricidal and antimicrobial activity of mononuclear phagocytes, granulocytes and NK cells. The activation of neutrophils by IFN-y includes an increase in their respiratory burst. IFN-y stimulates the cytolytic activity of NK cells. It is an activator of vascular endothelial cells, promoting CD4+ T lymphocyte adhesion and morphological alterations, which facilitates lymphocyte extravasation. IFN-y promotes opsonization by stimulating the production of IgG subclasses that activate the complement pathway. A summary of the characteristics of selected cytokines is shown in Table 2.3. 

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. 

Despite the well-studied respiratory burst it is now clear that superoxide is also released by a variety of non-phagocytic cells. For example human B-lympho-cytes, which have been transformed by Epstein-Barr virus, express a super-oxide-generating system similar in many respects to the NADPH-oxidase of neutrophils [80]. This oxidase in lymphocytes can be stimulated by cytokines, suggesting that superoxide release may be a normal function of these B-lympho-cytes [81], NADPH-oxidase also occurs in normal peripheral B-lymphocytes, but disappears from the cell surface during final differentiation to plasma cells. 

Superoxide is also a product of various enzyme reactions catalyzed by the flavin oxidases (e.g., xanthine oxidase and monoamine oxidase). In addition, 07 is a product of the noncatalytic oxidation of oxyhemoglobin, of which about 3% is converted each day to methemoglobin. Moreover, 02 is readily formed in phagocytic cells (i.e., neutrophils and monocytes) during the respiratory burst. Furthermore, in addition to the Fenton reaction, the Haber-Weiss reaction results in the conversion of 02 to the potent HO via the following reactions (H3) ... 

Principle The respiratory burst of phagocytic cells can be assessed by incubating a suspension of the cells in an isotonic solution of the yellow oxidised nitroblue tetrazolium (NBT) dye. During this process, the soluble dye interacts with the cytoplasmic components associating with the oxidant species generated. Although the NBT test is not a specific marker for superoxide production, NBT reduction by activat-... 

It is well-established that a major response to septic stimuh in general is the activation (primarily by cytokines and bacterial products, conditions that as described above also can induce NO synthesis) of phagocytic cells (neutrophils, macrophages) to produce ROS, through the respiratory burst mechanism this is a major immune mechanism for combating infectious agents but also can be damaging to the host. 

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