# Co-culture metabolomics: a powerful tool for uncovering host-pathogen phenotypes driving Burkholderia infections

## TL;DR

This study uses co-culture metabolomics to explore how Burkholderia pseudomallei infections affect host and bacterial metabolism, revealing potential new treatment targets for melioidosis.

## Contribution

The study introduces co-culture metabolomics as a novel method to uncover host-pathogen metabolic interactions during Burkholderia infections.

## Key findings

- Host pathways like polyamine biosynthesis and the tricarboxylic acid cycle are altered during Burkholderia infection.
- Bacterial metabolites such as methylated nucleotide bases and peptidoglycan precursors are affected by infection.
- Co-culture metabolomics can reveal new therapeutic strategies for melioidosis.

## Abstract

Melioidosis, caused by the soil-dwelling pathogen Burkholderia pseudomallei (Bt), is a severe respiratory infection with limited treatment options. To investigate the host-pathogen metabolic interplay occurring during these intracellular infections, Hicks et al. built upon an in vitro co-culture model they developed with airway epithelial cells and Bt as a surrogate pathogen (D. J. Hicks, N. Aiosa, A. Sinha, O. A. Jaiyesimi, et al., mSystems 10:e00611-25, 2025, https://doi.org/10.1128/msystems.00611-25). Using an untargeted metabolomics approach tailored to central metabolism, they identified several host pathways that were altered during the Bt infection: polyamine biosynthesis, nicotinamide adenine dinucleotide salvage, and the tricarboxylic acid cycle. In addition, they found that several bacterial metabolites, including methylated nucleotide bases, peptidoglycan precursors, and amino acid derivatives, were altered due to Bt infection. These results show that co-culture metabolomics is an effective strategy for identifying host-pathogen metabolic phenotypes resulting from bacterial infections and can uncover new therapeutic strategies to combat melioidosis.