Phagocytic ability function

Mechanisms by which ozone might interfere with bactericidal function include an alteration in cell-membrane function that produces a loss in phagocytic ability and is perhaps mediated by lipid peroxides and a decrease in the ability of veolar macrophages to kill phagocytized bacteria. Leukocytes in general appear to have a multiplicity of mechanisms for destroying ingested bacteria. 

Steroids also alter important functional activities of lymphocytes and monocytes. This effect is mainly on T lymphocytes and is at least partly due to a decrease in IL-2 production. Other proinflammatory cytokines such as IL-1 and IL-6 are also down regulated (Barnes, 2001 Krensky et al., 2005). The effect on B lymphocytes is less prominent. Steroids also profoundly impair the function of monocytes/macrophages by significantly decreasing their phagocytic ability. Glucocorticoids also increase I B expression, thereby curtailing activation of NF-kB, which increases apoptosis of activated cells (Auphan etal., 1995). 

There are three different kinds of lymphocytes that have specific functions T cells, B cells and NK cells. T cells develop in the thymus while B cells develop in the adult bone marrow. The thymus and the bone marrow are the primary lymphoid organs where lymphocytes acquire specific cell surface receptors that give them the ability to recognize antigens. NK cells are cytotoxic lymphocytes that develop in the bone marrow. The phagocytes are made up of either monocytes (macrophages) or polymorphonuclear granulocytes, which include neutrophils, eosinophils and basophils. 

Colchicine does not influence the renal excretion of uric acid or its concentration in blood. By virtue of its ability to bind to tubulin, colchicine interferes with the function of the mitotic spindles and causes depolymerization and disappearance of the fibrillar microtubules in granulocytes and other motile cells. This action is apparently the basis for the beneficial effect of colchicine, namely, the inhibition of the migration of granulocytes into the inflamed area and a decreased metabolic and phagocytic activity of granulocytes. This reduces the release of lactic acid and proinflammatory enzymes that occurs during phagocytosis and breaks the cycle that leads to the inflammatory response. 

The presence of edema and increased skin fragility (often the site of entrance of bacteria) are among the causes of increased risk of infections in nephrotic syndrome. Losses of immunoglobulin G and factor B (from the alternative pathway of the activation of complement) into the urine weaken the ability of the defense system to respond mainly to encapsulated microbes like pneumococci. The function of lymphocytes can be further weakened as a consequence of losses of zinc and transferrin into the urine. Weakening of the phagocytic function of macrophages has been described as well. 

Conneely, 2001). LF has the ability to bind to the surface of several types of immune cells, which suggests that it can modulate immune functions. Both stimulatory and inhibitory effects of LF on lymphocyte proliferation have been described in the literature. LF has been reported to induce in vitro maturation of T- and B-lymphocytes, to modulate the activity of natural killer cells and to enhance the phagocytic activity of neutrophils. In mice, bovine LF has been shown to induce both mucosal and systemic immune responses (Debbabi et al., 1998). Cell-culture studies have demonstrated that LF and peptides derived from LF influence the production of various cytokines which regulate the immune and inflammatory responses of the body (Crouch et al., 1992 Shinoda et al., 1996). 

---