Inflammation is a fundamental defensive response to harmful stimuli. However, it 
can cause damage if it does not subside. To avoid such damage, organisms have 
developed a mechanism called resolution of inflammation. Here we applied an 
untargeted metabolomics approach to a sterile and self-resolving animal model of 
acute inflammation, namely zymosan-induced peritonitis in mice, to examine the 
effect of inflammation and resolution on the metabolomic profiles. Significant 
and time-dependent changes in metabolite profiles after zymosan administration 
were observed in both peritoneal wash fluid (PWF) and plasma. These metabolomic 
changes correlated well with inflammatory chemokine or cytokine production. In 
PWF, most of metabolites that could detected increased in zymosan-treated mice, 
which is suggestive of inflammation, oxidative stress and increased energy 
demands. In plasma, most metabolites in the central metabolic pathway 
(glycolysis and TCA cycle) were significantly downregulated after zymosan 
administration. The concentration of the ketone body 3-hydroxybutyric acid 
(3-HB) in plasma and PWF increased in zymosan-injected animals indicating 
upregulation of fatty acid β-oxidation. Increased 3-HB level was observed in the 
cells that infiltrated into the peritoneal cavity and these infiltrated cells 
might contribute, at least in part, to the production of 3-HB in the peritoneal 
cavity.