Metabolomic profiling of LPS-induced systemic inflammation in mice: tryptophan as a biomarker for nutritional and inflammatory status.

Abstract

Lipopolysaccharide (LPS)-induced inflammation triggers metabolic reprogramming and nutritional decline. This study aimed to identify biomarkers for inflammatory and nutritional stress using gas chromatography-mass spectrometry (GC-MS/MS)-based metabolomic profiling. Male mice received LPS to induce systemic inflammation. Evaluations included liver histology (H&E, Gr-1), blood biochemistry, and metabolomic analysis of liver and plasma. LPS administration significantly increased hepatic neutrophil infiltration and liver enzymes, while decreasing nutritional markers (total protein, albumin, LDL-cholesterol). In the liver, LPS increased glycolytic and TCAcycle intermediates (e.g. 3-phosphoglycerate, citric acid) but decreased amino acids, including glutamine and tryptophan. Plasma analysis showed significant decreases in tryptophan, glucose, and succinic acid. Notably, tryptophan was significantly reduced in both compartments. Our findings demonstrate that tryptophan serves as a robust biomarker for monitoring the intersection of inflammatory response and nutritional status, reflecting synchronized metabolic shifts in the liver and plasma.