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Review
. 2024 Oct 23;12(11):2429.
doi: 10.3390/biomedicines12112429.

Modulation of the Immune Environment in Glioblastoma by the Gut Microbiota

Affiliations
Review

Modulation of the Immune Environment in Glioblastoma by the Gut Microbiota

George B H Green et al. Biomedicines. .

Abstract

Studies increasingly support the role of the gut microbiota in glioma development and treatment, although the exact mechanisms remain unclear. Research indicates that the gut microbiota can influence glioma progression, response to therapies, and the effectiveness of treatments like immunotherapy, with certain microbial compositions being linked to better outcomes. Additionally, the gut microbiota impacts the tumor microenvironment, affecting both tumor growth and the response to treatment. This review will explore glioma, the gut microbiota, and how their interaction shapes glioma development and therapy responses. Additionally, this review examines the influence of gut microbiota metabolites, such as short-chain fatty acids (SCFAs) and tryptophan, on glioma development and treatment. It also explores gut microbiome signaling via pattern recognition receptors, and the role of molecular mimicry between microbial and tumor antigens in glioblastoma, and if these interactions affect glioma development and treatment.

Keywords: glioblastoma; glioma; microbiome.

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Conflict of interest statement

The authors report no knowledge of any conflicts of interest.

Figures

Figure 1
Figure 1
Summary of the relationship among the microbiome, metabolome, brain, and glioblastoma. Abbreviations: Histone deacetylase (HDAC), M2 Macrophage (M2), Interleukin-10 (IL-10), Transforming growth factor beta (TGFβ), Vascular endothelial growth factor (VEGF), Perforin (Prf), Granzyme B (GzmB), Interferon gamma (IFNγ), Tumor necrosis factor alpha (TNFα), Akkermansia muciniphila (A. muciniphila), Bifidobacterium pseudolongum (B. pseudolongum), Adenosine A2a receptor (A2AR), T helper 1 cell (TH1), Anti-cytotoxic T-lymphocyte-associated protein 4 (α-CTLA4), Bacteroides fragilis (B. fragilis), Polysaccharide A (PSA), Toll-like receptor 2 (TLR2), Toll-like receptor 4 (TLR4), Interleukin-12 (IL-12), Lipopolysaccharide (LPS), Nuclear factor-kappa B (NF-κB), Dendritic cell (DC), Lipoteichoic acid (LTA), and T cell receptor (TCR). Created in BioRender. Cox, A. (2024) BioRender.com/u44g091. Available online: https://app.biorender.com/citation/67165b1fe8646874611b6bae (accessed on 20 October 2024).
Figure 2
Figure 2
The interaction among metabolites, immune cells, glioblastoma, and the brain. Abbreviations; Short-chain fatty acids (SCFAs), Gut-associated lymphoid tissue (GALT), Blood–brain barrier (BBB), Peroxisome proliferator-activated receptor gamma (PPAR-γ), Adenosine triphosphate (ATP), Regulatory T cell (Treg), Interleukin-10 (IL-10), Transforming growth factor beta (TGF-β), Perforin (Prf), Granzyme B (GzmB), Interferon gamma (IFNγ), and Tumor necrosis factor alpha (TNFα). Created in BioRender. Cox, A. (2024) BioRender.com/z29n756. Available online: https://app.biorender.com/citation/67165a3089a5793f6ce9b641 (accessed on 20 October 2024).

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