Abstracto
- Neuroimmune regulation of inflammation is only beginning to be explored in depth. In the case of amebiasis, the inflammatory process prompted by E. histolytica has been well characterized, but the modulation of this process by neurotransmitters is not as well defined. Regarding the inflammatory process, it is known that neutrophils and macrophages are important cellular effectors in the host defense against E. histolytica. The production of proinflammatory cytokines (IL-1β, IL-8, INF-γ and TNF-α) and anti- inflammatory cytokines (IL-10 and TGF-β) is triggered by the activation of Toll-Like Receptors and two types of transcription factors: 1) nuclear factor kappa-light-chain- enhancer of activated B cells, and 2) activator of transcriptions: Toll-Like Receptors and these transcription factors are in turn modulated by the action of three neurotransmitters of the autonomous nervous system acetylcholine, adrenaline and noradrenaline that can activate cholinergic and adrenergic receptors of immune cells, and thus modify the inflammatory process induced by the parasite. A vagotomy of the liver of hamsters inoculated with E. histolytica induces a stronger response in tissues through a more abundant formation of collagen, together with an increase in the levels of IL-10 and INF- γ and a decrease in macrophages, which impedes the dissemination of trophozoites.