The Effects of Probiotic Formulation Pretreatment (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) on a Lipopolysaccharide Rat Model

Abstract

Objective: The role of gut microbiota in the pathogenesis of several neurodegenerative disorders, including Alzheimer’s disease (AD), via the gut–brain axis has recently been demonstrated; hence, modification of the intestinal microbiota composition by probiotic biotherapy could be a therapeutic target for these conditions. The aim of this study was to assess the effects of a probiotic formulation (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) on inflammatory and memory processes in lipopolysaccharide (LPS)-induced rats, one of the animal models used in peripherally induced neuroinflammation and neurodegeneration.

Methods: Rats were randomly divided into four groups (Control, LPS, Probiotic + LPS, and Probiotic). All experimental groups were orally administrated maltodextrin (placebo) or probiotic (10⁹ CFU/ml/rat) for 14 consecutive days and then were injected with saline or LPS (1 mg/kg, intraperitoneally [i.p.], single dose) 20 hours later. Memory retention ability and systemic and neuroinflammatory markers were assessed 4 hours after the injections.

Results: Systemic exposure to LPS resulted in significant elevation of both the circulating and hippocampal levels of proinflammatory cytokines, which decreased remarkably following probiotic pretreatment. Oral bacteriotherapy with a combination of L. helveticus R0052 and B. longum R0175 also attenuated the decremental effect of LPS on memory through brain-derived neurotrophic factor (BDNF) expression at the molecular level; however, this effect was not significant in the passive avoidance test at the behavioral level.

Conclusions: These results suggest that the management of gut microbiota with this probiotic formulation could be a promising intervention to improve neuroinflammation-associated disorders such as AD.

Keywords:

• Probiotic
• lipopolysaccharide
• neuroinflammation
• memory
• Alzheimer’s disease

Acknowledgments

This work was supported by the Vice Chancellor of Research, Qazvin University of Medical Sciences (grant 28.20.13248). The authors are thankful to NeuroBiology and Neuroscience Research Centers, Shahid Beheshti University of Medical Sciences, for scientific and technical support. The results described in this article are part of Ghazaleh Mohammadi’s PhD work.

Disclosure statement

The authors declare that they have no competing interests.