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Phagocytosis, enhancement

Complement C3 1.2 cellophane mineral oil S. aureus granulocytes neutrophils neutrophils acute leukopenia (2) phagocytosis enhanced (3) attachment enhanced (4)... [Pg.233]

Immunoglobulin G 10-30 glass polvvinyl toluene PHEMA-PEMA platelets leucocytes fibroblasts and red cells adhesion and release enhanced (5) phagocytosis enhanced (6) adhesion prevented (7)... [Pg.233]

Cold insoluble globulin 0.1-0.3 falcon dishes RE-test emulsion PVC fibroblasts macrophages platelets adhesion enhanced (8) phagocytosis enhanced (9) thrombus enhanced (10)... [Pg.233]

PS-Ill arabino-p-3,6-galactan 35,000 phagocytosis enhancing activity Calendula officinalis L., flowers 1989 [89]... [Pg.167]

Table 1 - Chinese traditional drugs and herbs with phagocytosis enhancing activity ... Table 1 - Chinese traditional drugs and herbs with phagocytosis enhancing activity ...
Inhibition of inflammatory cytokines (Fig. 2) Humanized monoclonal anti-TNF antibodies (Infliximab (Remicade ), Adalimumab (Humira )) bind with high selectivity to human TNF-a and neutralize its activity. Thereby, infliximab decreases the effects of enhanced TNF levels during inflammatory disease such as production of proteases, chemokines, adhesion molecules, cyclooxygenase products (prostaglandins), and proinflammatory molecules such as interleukin-1 and -6. The antibodies may also recognize membrane-bound TNF-a on lymphocytes and other immune cells. These cells may subsequently become apoptotic or are eliminated via Fc-receptor-mediated phagocytosis. [Pg.412]

Peterson PK, Sharp BM, Gekker G, Jackson B, Balfour HH Jr (1991) Opiates, human peripheral blood mononuclear cells, and HIV. Adv Exp Med Biol 288 171-178 Peterson PK, Gekker G, Schut R, Hu S, Balfour HH Jr, Chao CC (1993) Enhancement of HlV-1 replication by opiates and cocaine the cytokine connection. Adv Exp Med Biol 335 181-188 Peterson PK, Gekker G, Hu S, Sheng WS, Molitor TW, Chao CC (1995) Morphine stimulates phagocytosis of Mycobacterium tuberculosis by human microglial cells involvement of a G protein-coupled opiate receptor. Adv Neuroimmunol 5 299-309 Peterson PK, Molitor TW, Chao CC (1998) The opioid-cytokine connection. J Neuroimmunol 83 63-69... [Pg.374]

When a microorganism breaches the iititial barriers and enters the body tissues, the phagocytes form a formidable defence barrier. Phagocytosis is greatly enhanced by a family of proteins called complement. [Pg.281]

The serum concentration of a number of proteins increases dramatically during infection. Their levels can increase by up to 100-fold compared with normal levels. They are known collectively as acute phase proteins and certain of them have been shown to enhance phagocytosis in conjunction with complement. [Pg.281]

It has the ability to cross the placenta and therefore provides a major line of defence against infection for the newborn. This can be reinforced by transfer ofcolostral IgG across the gut mucosa of the neonate. It diffuses readily into the extravascular spaces where it can act in the neutralization of bacterial toxins and can bind to microorganisms enhancing the process of phagocytosis (opsonization). This is due to the presence on the phagocytic cell surface of a receptor for Fc. [Pg.290]

Figure 8.9 Increased expression of IgG Fc receptors on phagocytes results in enhanced phagocytosis. These receptors will retain opsonized (i.e. antibody-coated) infectious agents at their surface by binding the Fc portion of the antibody. This facilitates subsequent phagocytosis... Figure 8.9 Increased expression of IgG Fc receptors on phagocytes results in enhanced phagocytosis. These receptors will retain opsonized (i.e. antibody-coated) infectious agents at their surface by binding the Fc portion of the antibody. This facilitates subsequent phagocytosis...
Immunoglobulins (Igs) can activate the complement system, which amplifies the immune response by enhancing chemotaxis, phagocytosis, and release of lymphokines by mononuclear cells that are then presented to T lymphocytes. The processed antigen is recognized by the major histocompatibility complex proteins on the lymphocyte surface, resulting in activation of T and B cells. [Pg.44]

Wizemann, T.M. and Laskin, D.L. Enhanced phagocytosis, chemotaxis, and production of reactive oxygen intermediates by interstitial lung macrophages following acute endo-toxemia, Am. J. Respir. Cell Mol. Biol., 11, 358, 1994. [Pg.121]

Collectins Alveolar type II cells and non-ciliated bronchiolar epithelial cells Bacterial and fungal cell walls and viruses Enhance phagocytosis of macrophages and neutrophils activating cells Cigarette smoke decreases the production of collectin [48] ozone decreases function [49]... [Pg.310]

Schagat, T.L., Wofford, J.A., and Wright, J.R., Surfactant protein A enhances alveolar macrophage phagocytosis of apoptotic neutrophils, J. Immunol. 166, 4, 2727, 2001. [Pg.320]

LeVine, A.M., et al., Surfactant protein-A binds group B streptococcus enhancing phagocytosis and clearance from lungs of surfactant protein-A-deficient mice, Am. J. Respir. Cell Mol. Biol. 20, 2, 279, 1999. [Pg.320]

Humoral immunity is characterized by the production of antigen-specific antibodies that enhance phagocytosis and destruction of microorganisms through opsonization. Thus, deficiencies of humoral immunity (B lymphocytes) may lead to reduced antibody titers and are typically associated with acute gram-positive... [Pg.542]

Since cellular immunity results in the release of chemotactic lymphocytes that in turn enhance phagocytosis, a deficiency in cellular immunity may also result in chronic infections. Cellular immunity is mediated by T cells, macrophages, and NK cells involved in complex compensatory networks and secondary changes. Immunosuppressive agents may act directly by lethality to T cells, or indirectly by blocking mitosis, lymphokine synthesis, lymphokine release, or membrane receptors to lymphokines. In addition, cellular immunity is involved in the production and release of interferon, a lymphokine that ultimately results in blockage of viral replication (Table 15.4). Viruses are particularly susceptible to cytolysis by T cells since they often attach to the surface of infected cells. Thus, immunosuppression of any of the components of cellular immunity may result in an increase in protozoan, fungal, and viral infections as well as opportunistic bacterial infections. [Pg.543]


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