Info

No induction and production

The major effects are indicated in bold. Th-1, lymphocytes T CD4 auxiliary; Th-2, lymphocytes T CD4 inflammation; CTL, lymphocyte T CD8 cytotoxic; MHC, major histocompatibility complex.

Interleukin-10

liiterleukiii-12

Interferon-c

TNF-a

Lymphocytes

(Th-2) Macrophages, dendritic cells Lymphocytes (Th-1, CLL)

Increase MHC II

Differentiation IgG synthesis

Inhibit Th-1 Differentiation

Death

Inhibit cytokine release

Activation INCREASE MHC I and II NO activation.

Costimulate mastocyte growth

NK cell activation

Antiviral, increase MHC I and II

NK cells and the expression of cytokines, such as the interferon-g and the transforming growth factor-b. It has recently been suggested that polyamines could inhibit the synthesis of NO because the metabolisms of polyamines and NO are partly interconnected via a common precursor, l- a rginine (Fig. 2) ( 52,53). Furthermore, NO could inhibit polyamine biosynthesis through the nitrosylation of the active ODC site (54,55). Finally, spermine was found to inhibit iNOS expression in LPS-treated macrophages J774.2 (53).

Taken together, many observations support the notion that polyamines are antiinflammatory molecules. However, numerous studies were in a cell culture environment, which contains bovine serum and, thus, artificially high concentration of polyamine oxidase. This enzyme is well known to produce toxic byproducts of polyamines that could be at the origin of the anti-inflammatory effects of polyamines. Given the detrimental role of polyamines in excitotoxicity models in vivo and its potential involvement in neurodegenerative diseases, the following section presents the role of polyamines in the brain in vivo.

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