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Fig. 1. Mediators of innate immunity and polyamines. This figure depicts a central role of macrophages in the innate immune response and the potential involvement of polyamines in these events. Macrophages are first activated by pathogen components, called pathogen-associated molecular patterns. Then myeloid cells release proinflammatory cytokines (TNF-a, interleukin 1, interleukin 12), which can activate natural killer (NK) cells. NK cells release the cytokine interferon-g (IFN-g), which further stimulates macrophages. A chemoattractant gradient takes place in response to the chemokine production by macrophages and endothelial cells. Neutrophils and monocytes are attracted from the lumen of the blood vessels to the parenchyma where the area of infection is located. Once into the parenchyma, monocytes differentiate into macrophages. Activated macrophages induce the adaptive immunity via the stimulation of B- and T-cells. This transfer from innate to adaptive immunity is highly dependent on interleukin-12. Macrophages play, therefore, a critical role in the control of the innate immune response and polyamines have a major impact on these events because of their ability to modulate the release of various proinflammatory molecules.

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