Vagotomy Induces Deregulation of the Inflammatory Response during the Development of Amoebic Liver Abscess in Hamsters

Background: The parasympathetic nervous system modulates the immune response in the abdominal-pelvic gut through the vagus nerve, which releases acetylcholine. This endogenous ligand acts on alpha 7 nicotinic receptors expressed on immune cells. Objective: To study the mechanism of the production and regulation of cytokines in parasympathectomized and control hamsters during the development of amoebic liver abscesses (ALA) caused by Entamoeba histolytica. Methodology: Six-to 8-week-old male hamsters with and without vagotomy were used in a model of ALA. The animals were infected with trophozoites (350,000; HM1: IMSS strain) via the intrahepatic route and sacrificed at 6, 12, and 24 h and at 2, 4, and 7 days postinfection. Immune parameters were recorded at each time point using morphometric techniques including immunofluorescence and immunohistochemistry assays. These parameters included signal transducer and activator of transcription 3 (STAT3) levels, pro-and anti-inflammatory cytokine levels, and nuclear factor-kappa B (NF kappa B) activation in neutrophils and macrophages. Results: Compared to the control groups, the vagotomized (VAG) hamsters showed a significant increase in NF kappa B activation in neutrophils and macrophages, and higher levels of interleukin (IL)-1 beta, IL-6, interferon-gamma, and tumor necrosis factor-alpha. VAG hamsters showed an increase in the expression of IL-8 and phosphorylated STAT3 during the first 24 h postinfection as well as slightly increased levels of transforming growth factor-beta on days 2-7 postinfection. No significant differences were demonstrated in the levels of IL-10. Conclusions: These results suggest that the vagus nerve plays an important role in the regulation of inflammation during ALA formation. (C) 2014 S. Karger AG, Basel