# Metabolic changes in dorsal root ganglia of newborn Wistar rats following LPS exposure to understand mechanisms of critical illness polyneuropathy

**Authors:** Amandine Szczesnowski, Christelle Le Gall‐Ianotto, Marie‐Dominique Jezequel, Michaël Théron, Karelle Léon, Karine Pichavant‐Rafini

PMC · DOI: 10.14814/phy2.70633 · Physiological Reports · 2025-11-02

## TL;DR

This study explores how LPS exposure affects the metabolism of nerve cells in newborn rats, potentially shedding light on a complication of sepsis called critical illness polyneuropathy.

## Contribution

The study reveals novel insights into how LPS-induced inflammation and mitochondrial dysfunction may contribute to metabolic changes in dorsal root ganglia cells.

## Key findings

- LPS exposure at higher concentrations significantly increased IL-6 release and altered mitochondrial and glycolytic metabolism.
- Adaptive responses in DRG cells were observed at specific LPS concentrations, indicating potential mechanisms for metabolic disturbances.
- Gene expression trends in SOD2 and Fis1 suggest a link between mitochondrial function and inflammation in LPS-exposed cells.

## Abstract

Sepsis is a public health issue, associated with complications as critical illness polyneuropathy (CIP). This study investigates how mitochondrial dysfunction could contribute to CIP by examining metabolic changes in dorsal root ganglia (DRG) culture from newborn Wistar rats exposed to different concentrations of lipopolysaccharide (5, 10, 50, and 100 μg/mL for 24 or 48 h). Cell viability was assessed using the MTS assay, gene expression related to inflammation and mitochondrial function was analyzed by Real‐Time PCR. IL‐6 levels of supernatants were measured by ELISA and energetic metabolism was evaluated with the Seahorse MitoStress kit. Exposure to LPS at varying concentrations mainly did not affect cell viability, except at 10 μg/mL for 48 h, where a 7.5% increase was noted. Gene expression analysis showed trends in SOD2 and Fis1, with significant increases in IL‐6 and LIF transcripts at 5 and 10 μg/mL. IL‐6 release was significant at 50 and 100 μg/mL of LPS. Mitochondrial respiration and glycolytic metabolism exhibited significant changes in oxygen consumption rate and extracellular acidification, particularly at higher LPS concentrations. The findings suggest that LPS induces an inflammatory environment which led to metabolic disturbances in DRG cells, with adaptive responses at 10 and 50 μg/mL of LPS.

## Linked entities

- **Genes:** SOD2 (superoxide dismutase 2) [NCBI Gene 6648], FIS1 (fission, mitochondrial 1) [NCBI Gene 51024], IL6 (interleukin 6) [NCBI Gene 3569], LIF (LIF interleukin 6 family cytokine) [NCBI Gene 3976]
- **Diseases:** critical illness polyneuropathy (MONDO:0001957), CIP (MONDO:0009459)

## Full-text entities

- **Genes:** Il6 (interleukin 6) [NCBI Gene 24498] {aka ILg6, Ifnb2}, Fis1 (fission, mitochondrial 1) [NCBI Gene 288584] {aka Ttc11}, Sod2 (superoxide dismutase 2) [NCBI Gene 24787] {aka MnSOD}, Lif (LIF, interleukin 6 family cytokine) [NCBI Gene 60584]
- **Diseases:** mitochondrial dysfunction (MESH:D028361), inflammation (MESH:D007249), Sepsis (MESH:D018805), CIP (MESH:D011115)
- **Chemicals:** LPS (MESH:D008070), oxygen (MESH:D010100)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12580404/full.md

## References

47 references — full list in the complete paper: https://tomesphere.com/paper/PMC12580404/full.md

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Source: https://tomesphere.com/paper/PMC12580404