# High-Seas Marine Microorganism Delivers an Extract That Dampens LPS-Driven Pro-Inflammatory Signaling: Galbibacter orientalis Strain ROD011

## TL;DR

A deep-sea bacterium produces an extract that significantly reduces inflammation in cells and zebrafish embryos without harming them.

## Contribution

The study identifies a novel anti-inflammatory extract from a deep-sea microorganism and reveals its metabolic mechanisms.

## Key findings

- GOEE reduced nitric oxide production by 72–87% in LPS-stimulated macrophages without cytotoxicity.
- GOEE suppressed COX-2 protein and attenuated LPS-induced signals in zebrafish embryos.
- Metabolomic analysis revealed 18 significant pathways involved in inflammation suppression.

## Abstract

An ethyl acetate extract from the deep-sea bacterium Galbibacter orientalis strain ROD011 (GOEE), collected from international waters, was investigated as a potential anti-inflammatory agent. In lipopolysaccharide (LPS)-stimulated murine macrophages, nitric oxide (NO) production fell by 72–87% at 5–20 µg/mL GOEE without detectable cytotoxicity. Cyclooxygenase-2 (COX-2 protein abundance decreased in a dose-dependent manner and was nearly absent at 20 µg/mL. In zebrafish embryos, survival was maintained up to 40 µg/mL, and LPS-induced signals were attenuated; the cell-death rate declined from 10 µg/mL onward, and at 20 µg/mL GOEE, reactive oxygen species (ROS) and NO decreased by 85% and 27%, respectively. To explain these effects, untargeted metabolomics with pathway enrichment and network mapping were performed in LPS-driven macrophages. Of the 58 KEGG pathways evaluated, 18 reached significance, notably purine and pyrimidine metabolism, vitamin B6 metabolism, and the one-carbon pool via folate. Coordinated shifts also involved amino-acid/tricarboxylic acid (TCA)-cycle linkages, glutathione and glyoxylate/dicarboxylate, and sphingolipid pathways. Network analysis identified hubs that were concomitantly reprogrammed. Collectively, GOEE achieved multi-level suppression of inflammatory outputs while preserving viability, and the metabolomic signature provides a mechanistic scaffold for its action. These findings nominate a deep-sea microbial extract as a promising anti-inflammatory lead and motivate fractionation and targeted validation of the highlighted metabolic nodes.