# Lipidome Disturbances of Vibrio alginolyticus Associated with Citral Exposure

## TL;DR

This study explores how citral, a natural compound, affects the lipid composition of Vibrio alginolyticus, a harmful bacteria in aquaculture.

## Contribution

The study reveals novel lipidome disturbances in V. alginolyticus caused by citral exposure and identifies key metabolic pathways involved.

## Key findings

- Citral exposure significantly altered the lipid composition of V. alginolyticus, including phospholipids and sphingolipids.
- Phospholipid content decreased while ceramides and lysophospholipids accumulated with increasing citral concentration.
- Lipid remodeling primarily involved phospholipid and sphingolipid metabolic pathways in response to citral.

## Abstract

Vibrio alginolyticus is an important antibiotic-resistant pathogen in aquaculture that can cause mortality in a wide range of aquatic animals and infect humans. It is urgently necessary to discover and develop effective antibiotic alternatives. Citral, a key antibacterial component of lemongrass oil, can be used as a food flavoring and additive. Although the antimicrobial activity and antibiofilm effect of citral against V. alginolyticus have been noted in our previous study, the potential lipidome influence of citral remains unclear. Accordingly, a non-targeted lipidomics approach was employed to investigate citral-induced lipidome disturbances and reveal potential regulated targets of citral against V. alginolyticus. We found that the citral exposure triggered substantial lipidome alterations (i.e., composition, contents, and structure) in V. alginolyticus. Specifically, the content of most phospholipids (e.g., phosphatidylcholines (PCs), phosphatidylethanolamines (PEs), phosphatidylserines (PSs), phosphatidylinositols (PIs), and phosphatidylglycerols (PGs)) decreased with the increase in citral concentration, while ceramides (Cers) and lysophospholipids (LPLs) (e.g., lyso-PAs, lyso-PCs, lyso-PEs, and lyso-PGs) showed concentration-dependent accumulation under citral treatment. Notably, the critical lipid remodeling in response to citral exposure mainly involved the phospholipid and sphingolipid metabolic pathways. Collectively, our study reveals the bacterial lipidome response to citral exposure and highlights pivotal metabolic pathways, potentially offering a novel perspective for future investigations into lipid-centric antibacterial targets.