Bifidobacterium pseudocatenulatum CECT 7765 Reduces Obesity-Associated Inflammation by Restoring the Lymphocyte-Macrophage Balance and Gut Microbiota Structure in High-Fat Diet-Fed Mice
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BACKGROUND/OBJECTIVES: The role of intestinal dysbiosis in obesity-associated systemic inflammation via the cross-talk with peripheral tissues is under debate. Our objective was to decipher the mechanisms by which intervention in the gut ecosystem with a specific Bifidobacterium strain reduces systemic inflammation and improves metabolic dysfunction in obese high-fat diet (HFD) fed mice. METHODS: Adult male wild-type C57BL-6 mice were fed either a standard or HFD, supplemented with placebo or Bifidobacterium pseudocatenulatum CECT 7765, for 14 weeks. Lymphocytes, macrophages and cytokine/chemokine concentrations were quantified in blood, gut, liver and adipose tissue using bead-based multiplex assays. Biochemical parameters in serum were determined by ELISA and enzymatic assays. Histology was assessed by hematoxylin-eosin staining. Microbiota was analyzed by 16S rRNA gene pyrosequencing and quantitative PCR. RESULTS: B. pseudocatenulatum CECT 7765 reduced obesity-associated systemic inflammation by restoring the balance between regulatory T cells (Tregs) and B lymphocytes and reducing pro-inflammatory cytokines of adaptive (IL-17A) and innate (TNF-α) immunity and endotoxemia. In the gut, the bifidobacterial administration partially restored the HFD-induced alterations in microbiota, reducing abundances of Firmicutes and of LPS-producing Proteobacteria, paralleled to reductions in B cells, macrophages, and cytokines (IL-6, MCP-1, TNF-α, IL-17A), which could contribute to systemic effects. In adipose tissue, bifidobacterial administration reduced B cells whereas in liver the treatment increased Tregs and shifted different cytokines (MCP-1 plus ILP-10 in adipose tissue and INF-γ plus IL-1β in liver). In both tissues, the bifidobacteria reduced pro-inflammatory macrophages and, TNF-α and IL-17A concentrations. These effects were accompanied by reductions in body weight gain and in serum cholesterol, triglyceride, glucose and insulin levels and improved oral glucose tolerance and insulin sensitivity in obese mice. CONCLUSIONS: Here, we provide evidence of the immune cellular mechanisms by which the inflammatory cascade associated with diet-induced obesity is attenuated by the administration of a specific Bifidobacterium strain and that these effects are associated with modulation of gut microbiota structure.
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Intestinal microbe composition and corresponding byproducts [e.g., short-chain fatty acids, (SCFA)] are associated with diabetes risk in clinical observations and have been shown to improve glycemic control in pre-clinical models.
“Intestinal microbe composition and corresponding byproducts [e.g., short-chain fatty acids, (SCFA)] are associated with diabetes risk in clinical observations (24) and have been shown to improve glycemic control in pre-clinical models (25).”
From Prebiotic soda lowers postprandial glucose compared to traditional soda pop: a randomized controlled trial (2025) · cites this paper as [25]
The citation (25) is attached to the pre-clinical glycemic-control claim, not the clinical-observation claim (24). In Results, “B. pseudocatenulatum CECT 7765 reduced metabolic alterations in obese mice” (page unavailable), the probiotic lowered serum glucose in high-fat-diet-fed mice, supporting that part. The paper does not establish that short-chain fatty acids or other microbial byproducts produced the improvement. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPrebiotics have the potential to improve glycemic control through gut microbiome modulation.
“Prebiotics have the potential to improve glycemic control through gut microbiome modulation, though this mechanism was not directly assessed in the present study.”
From Prebiotic soda lowers postprandial glucose compared to traditional soda pop: a randomized controlled trial (2025) · cites this paper as [25]
The Introduction (page unavailable) says prebiotics can alter gut Bifidobacterium numbers and have improved some obesity-associated metabolic alterations in animal models. The Results (page unavailable) report lower glucose in mice given B. pseudocatenulatum, but that intervention was a probiotic, not a prebiotic. The paper therefore supports the general possibility of metabolic benefits from microbiome modulation, but not the specific claim that prebiotics improve glycemic control through that mechanism. (LLM, conf=0.86)
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- Authors
- Moya-Pérez, A., Neef, A., & Sanz, Y.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Corresponding author
- Sanz, Yolanda
- Venue
- PLOS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2015-07-10
- Volume
- 10
- Issue
- 7
- Pages
- e0126976
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4498624
- OpenAlex
- W833377501
- Cited by
- 211
- References
- 5
- Citations by year
- 2026: 8 · 2025: 15 · 2024: 14 · 2023: 21 · 2022: 29 · 2021: 18 · 2020: 15 · 2019: 27 · 2018: 27 · 2017: 22 · 2016: 10 · 2015: 5
- FWCI
- 8.41
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RIUCV (Universidad Católica de Valencia San Vicente Martír) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Funders
- Universitat de València
- Ministerio de Ciencia e Innovación (CSD2007-00063)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- Bifidobacterium pseudocatenulatum, probiotics, diet-induced obesity, systemic inflammation, gut microbiota, regulatory T cells, B cells, macrophages, inflammatory cytokines, endotoxemia, lipopolysaccharide, insulin sensitivity, glucose tolerance, high-fat diet, adipose tissue, liver
- MeSH terms
- Gastrointestinal Microbiome, Animals, Bifidobacterium, Immunity, Cellular, Inflammation, Lymphocytes, Macrophages, Male, Mice, Inbred C57BL, Obesity, Weight Gain, Mice, Diet, High-Fat
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