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Purpose <p>Current antidepressants targeting neurotransmitters often fail to alleviate symptoms. Alternative hypotheses suggest inflammation may trigger an alternative route that converts tryptophan into kynurenine, reducing the bioavailability of tryptophan to synthesize serotonin while producing neuroactive metabolites such as quinolinic acid (QUINA, excitotoxic) and kynurenic acid (KYNA, neuroprotective). This study evaluates the effects on these systems of a specific strain of <i>Ligilactobacillus salivarius</i> (<i>L. salivarius</i>), identified in the Spanish Type Culture Collection as CECT 30632, in a preclinical model depression.</p> Methods <p>Male Wistar rats (<i>n</i> = 32) were divided into control (CT) and chronic mild stress (CMS) groups, treated with either vehicle or <i>L. salivarius</i> CECT 30632 for four weeks, starting one week before CMS exposure. Behavioral assessments, including the splash test (ST) and open field test (OF), were conducted. Biochemical analyses of peripheral blood mononuclear cells (PBMCs), plasma, and frontal cortex (FC) samples assessed antioxidant markers phospho-nuclear factor (erythroid-derived 2)-like 2 (p-Nrf2) and glutathione peroxidase 1 (GPx1), as well as tryptophan metabolites.</p> Results <p>In the ST, <i>L. salivarius</i> CECT 30,632 reduced latency to groom, indicating improved anhedonia and self-care, while no changes were observed in the OF test. CMS reduced p-Nrf2 and GPx1 expression in PBMCs, which was restored by <i>L. salivarius</i> CECT 30,632. This bacterium also reduced the QUINA/KYNA ratio in plasma and FC, suggesting a lower excitotoxicity risk.</p> Conclusion <p><i>Ligilactobacillus salivarius</i> CECT 30632 improved behavioral outcomes, enhanced antioxidant defenses, and modulated tryptophan metabolism in a rat model of CMS. These findings support its potential as a probiotic intervention for depression.</p>

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Behavioral, antioxidant, and kynurenine pathway modulation of a specific strain of Ligilactobacillus salivarius in a preclinical model of depression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月9日

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  • David Martín-Hernández,
  • Javier R. Caso,
  • César Díaz-García,
  • Pedro-Antonio Regidor,
  • José Miguel Rizo,
  • Marta Román,
  • Rocío Gutiérrez,
  • Juan Carlos Leza

摘要

Purpose

Current antidepressants targeting neurotransmitters often fail to alleviate symptoms. Alternative hypotheses suggest inflammation may trigger an alternative route that converts tryptophan into kynurenine, reducing the bioavailability of tryptophan to synthesize serotonin while producing neuroactive metabolites such as quinolinic acid (QUINA, excitotoxic) and kynurenic acid (KYNA, neuroprotective). This study evaluates the effects on these systems of a specific strain of Ligilactobacillus salivarius (L. salivarius), identified in the Spanish Type Culture Collection as CECT 30632, in a preclinical model depression.

Methods

Male Wistar rats (n = 32) were divided into control (CT) and chronic mild stress (CMS) groups, treated with either vehicle or L. salivarius CECT 30632 for four weeks, starting one week before CMS exposure. Behavioral assessments, including the splash test (ST) and open field test (OF), were conducted. Biochemical analyses of peripheral blood mononuclear cells (PBMCs), plasma, and frontal cortex (FC) samples assessed antioxidant markers phospho-nuclear factor (erythroid-derived 2)-like 2 (p-Nrf2) and glutathione peroxidase 1 (GPx1), as well as tryptophan metabolites.

Results

In the ST, L. salivarius CECT 30,632 reduced latency to groom, indicating improved anhedonia and self-care, while no changes were observed in the OF test. CMS reduced p-Nrf2 and GPx1 expression in PBMCs, which was restored by L. salivarius CECT 30,632. This bacterium also reduced the QUINA/KYNA ratio in plasma and FC, suggesting a lower excitotoxicity risk.

Conclusion

Ligilactobacillus salivarius CECT 30632 improved behavioral outcomes, enhanced antioxidant defenses, and modulated tryptophan metabolism in a rat model of CMS. These findings support its potential as a probiotic intervention for depression.