Endogenous acetylcholine controls the severity of polymicrobial sepsisassociated inflammatory response in mice

Flavio Almeida Amaral, Caio Tavares Fagundes, Aline Silva Miranda, Vivian Vasconceios Costa, Livia Resende, Danielle Da Gloria De Souza, Vania Ferreira Prado, Mauro Martins Teixeira, Marco Antonio Maximo Prado, Antonio Lucio Teixeira

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


Acetylcholine (ACh) is the main mediator associated with the anti-inflammatory cholinergic pathway. ACh plays an inhibitory role in several inflammatory conditions. Sepsis is a severe clinical syndrome characterized by bacterial dissemination and overproduction of inflammatory mediators. The aim of the current study was to investigate the participation of endogenous ACh in the modulation of inflammatory response induced by a model of polymicrobial sepsis. Wild type (WT) and vesicular acetylcholine transporter knockdown (VAChTKD) mice were exposed to cecal ligation and perforation- induced sepsis. Levels of Tumor Necrosis Factor Alpha (TNF-α) and bacterial growth in peritoneal cavity and serum, and neutrophil recruitment into peritoneal cavity were assessed. The concentration of TNF-α in both compartments was higher in VAChTKD in comparison with WT mice. VAChTKD mice presented elevated burden of bacteria in peritoneum and blood, and impairment of neutrophil migration to peritoneal cavity. This phenotype was reversed by treatment with nicotine salt. These findings suggest that endogenous ACh plays a major role in the control of sepsis-associated inflammatory response.

Original languageEnglish (US)
Pages (from-to)4-9
Number of pages6
JournalCurrent Neurovascular Research
Issue number1
StatePublished - Feb 1 2016
Externally publishedYes


  • Acetylcholine
  • Inflammation
  • Neutrophils
  • Nicotine
  • Sepsis

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience
  • Cellular and Molecular Neuroscience


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