Effects of spleen nerve denervation on depression–like phenotype, systemic inflammation, and abnormal composition of gut microbiota in mice after administration of lipopolysaccharide: A role of brain–spleen axis

Aug 29, 2022Journal of affective disorders

How Cutting Nerve Signals to the Spleen Affects Depression-Like Behavior, Body Inflammation, and Gut Bacteria in Mice After Immune Activation: Involvement of the Brain-Spleen Connection

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Abstract

Splenic nerve denervation blocked LPS-induced depression-like symptoms in mice.

LPS administration caused a depression-like phenotype and systemic inflammation in sham-operated mice.
In SND-operated mice, LPS did not produce depression-like symptoms or abnormal microglial and postsynaptic protein expressions in the hippocampus.
SND significantly reduced LPS-induced increases in plasma interleukin-6 levels, indicating anti-inflammatory effects.
Changes in gut microbiota composition were observed across different experimental groups.
Correlations were found between gut microbiota abundance and microglial activation markers in the hippocampus.

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BACKGROUND: Accumulating evidence suggests the role of brain-spleen axis as well as brain-gut-microbiota axis in inflammation-related depression. The spleen mediates anti-inflammatory effects of the vagus nerve which plays a role in depression. However, the role of spleen nerve in inflammation-related depression remains unclear.

METHODS: The effects of the splenic nerve denervation (SND) in the depression-like phenotype, systemic inflammation, and abnormal composition of gut microbiota in adult mice after administration of lipopolysaccharide (LPS) were examined.

RESULTS: LPS (0.5 mg/kg) caused depression-like phenotype, systemic inflammation, splenomegaly, increased expression of Iba1 (ionized calcium-binding adapter molecule 1) and decreased expression of postsynaptic density protein-95 (PSD-95) in the hippocampus in the sham-operated mice. In contrast, LPS did not produce depression-like phenotype, and abnormal expressions of Iba1 and PSD-95 in the hippocampus in the SND-operated mice. Furthermore, SND significantly blocked LPS-induced increased plasma levels of pro-inflammatory cytokine interleukin-6 although SND did not affect LPS-induced splenomegaly and increased plasma levels of tumor necrosis factor-α in mice. There were significant changes in several microbiota among the four groups. Interestingly, there were correlations between the relative abundance of several microbiota and Iba1 (or PSD-95) expression in the hippocampus. In addition, expression of Iba1 in the hippocampus was correlated with the relative abundance of several microbiota.

LIMITATIONS: Detailed mechanisms are unclear.

CONCLUSIONS: These results suggest that the splenic nerve plays a role in inflammation-related depression, microglial activation in the hippocampus, and that gut microbiota may regulate microglial function in the brain via gut-microbiota-brain axis.

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Effects of spleen nerve denervation on depression–like phenotype, systemic inflammation, and abnormal composition of gut microbiota in mice after administration of lipopolysaccharide: A role of brain–spleen axis

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