Macrophage assay

Utilizing a pulmonary macrophage assay, most lanthanides appeared to be less toxic... 

The third mechanism is the FcR-mediated phagocytosis upon antibody binding to its cellular receptor targets on macrophages. Assays based on phagocytosis are very difficult to standardize and use for potency determination. 

Acute mammalian Colony Forming Unit-Granulocyte/Macrophage Assay for acute neutropenia in humans In vitro... 

Colepicolo, P., et al. (1990). A sensitive and specific assay for superoxide anion released by neutrophils or macrophages based on bioluminescence of polynoidin. Anal. Biochem. 184 369-374. 

The antiinflammatory effects of statins likely result from their ability to inhibit the formation of mevalonic acid. Downstream products of this molecule include not only the end product, cholesterol, but also several isoprenoid intermediates that covalently modify ( pre-nylate ) certain key intracellular signaling molecules. Statin treatment reduces leukocyte adhesion, accumulation of macrophages, MMPs, tissue factor, and other proinflammatory mediators. By acting on the MHC class II transactivator (CIITA), statins also interfere with antigen presentation and subsequent T-cell activation. Statin treatment can also limit platelet activation in some assays as well. All these results support the concept that in addition to their favorable effect on the lipid profile, statins can also exert an array of antiinflammatory and immunomodulatory actions. 

Urethane hydrolyzes into an amine, an alcohol, and carbon dioxide. So the possible degradation products of a poly(phosphoester-urethane) are diamines, diols, phosphates, carbon dioxide, and even ureas. Urea is possible because the isocyanate is extremely sensitive to moisture, which would convert the isocyanate to an amino group. One is therefore bound to have traces of diamine in the polymerization that leads to a urea bond in the backbone. We think the cytotoxicity seen in the macrophage functional assay comes from the TDI structure. 

Interferon-y (IFN-y) mRNA levels were measured in unstimulated peripheral blood mononuclear cell (PBMC) and purified cell populations, using a bDNA assay, to characterize the cell types that contribute to the in vivo increase in IFN-y gene expression seen in HIV infection (Breen et al 1997). IFN-y is a cytokine that can be produced by multiple cell types and is considered to enhance cellular responses by activation of monocytes and macrophages. It is one of the type 1 cy-... 

Haematotoxicity The colony forming unit-granulocyte/ macrophage (CFU-GM) assay for predicting acute neutropenia in humans EU... 

Bonfield, T.L., John, N., Bama, B.P., Kavuru, M.S., Thomassen, M.J., and Yen-Lieberman, B. (2005) Multiplexed particle-based anti-granulocyte macrophage colony stimulating factor assay used as pulmonary diagnostic test. Clin. Diagn. Lab. Immunol. 12, 821-824. 

Fig. 8.8 Macrophage cytotoxic assays of plant extracts. Supernatant samples were tested from Trgeneration of chloroplast transgenic line pLD-JWl (proteins were extracted in buffer containing no detergent and MTTwas added after 5 hours). pLD-JWl (extract stored for 2 days) pLD-JWl (extract stored for 7 days) -> PA 5 pg ml-1 —x— Control wild type (extract stored for 2 days) ...

Figure 9.3 Activation of T-cells by interaction with macrophage-displayed antigen. Activation results in IL-2 production, which acts in an autocrine manner to stimulate further T-cell growth and division. IL-2 thus represents the major regulatory molecule responsible for stimulation of cell-mediated immunity. Note that it was initially believed that binding of presented antigen alone was insufficient to trigger T-cell activation. It was thought that co-stimulation with IL-1 was reguired. However, the assay used to detect the co-stimulation was found not to be specific for IL-1 alone. The role of IL-1 as a co-stimulator of T-cell activation is now believed to be minimal at most...

Ex vivo studies have revealed that trichothecenes can both inhibit and stimulate leukocyte function.12 For example, trichothecenes are toxic to alveolar macrophages,13 but drive differentiation of human myeloid leukemic cells.14 Dose-dependent decreases or increases in B- and T-cell mitogen responses are observable in lymphocytes from animals exposed to T-2 toxin, DON, or various macrocyclic trichothecenes these toxins similarly impair or enhance mitogen-induced lymphocyte proliferation in vitro.12 Rank order of inhibitor potency in rodent and human lymphocyte proliferation assays is Type D > Type A group > Type B group and is dependent on degree of acylation as well as of uptake and metabolism. 

As described previously, the humoral immune response results in the proliferation, activation, and subsequent production of antibodies by B cells following antigenic exposure and stimulation. The functionality and interplay between the three primary types of immune cells (macrophage, B cells, and T cells) required to elicit a humoral response can be assessed through various in vitro assays using cells from the peripheral blood or lymphoid tissues. 

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