Regulating The Immune Response
For the first time (in 1987) in experiment it has been shown that armin (nonreversible inhibitor of acetylcholinesterase) at their injection 24 h prior to sepsis modelling invoke essential depression of a lethality of mice from experimental infectious process. Later (in 1995) this data has been confirmed at cholinergic stimulation by other cholinomimetics.
Tumor Necrosis Factor (TNF) (and other cytokines) are produced by cells of the innate immune system during local injury and infection. These contribute to initiating a cascade of mediator release, and recruiting inflammatory cells to the site of infection to contain infection, referred to as "innate immunity.". TNF amplifies and prolongs the inflammatory response by activating other cells to release interleukin-1 (IL-1), high mobility group B1 (HMGB1) and other cytokines. These inflammatory cytokine responses confer protective advantages to the host at the site of bacterial infection. A “beneficial” inflammatory response is limited, resolves in 48-72 hours, and does not spread systemically. The cholinergic anti-inflammatory pathway provides a braking effect on the innate immune response which protects the body against the damage that can occur if a localized inflammatory response spreads beyond the local tissues, which results in toxicity or damage to the kidney, liver, lungs, and other organs.
Read more about this topic: Cholinergic Anti-inflammatory Pathway
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