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Live Akkermansia muciniphila rescues exhausted CD8+ Cytotoxic T Lymphocytes (CTLs) , converting them into cytotoxic subpopulations critical for tumor cell killing
The effect is achieved by disrupting immunosuppressive interactions. These occur in the tumor microenvironment. An example is the Chemokine (C-X-C motif) ligand 3 (CXCL3)-CD274 (Programmed death-ligand 1 (PD-L1)) axis. This axis exists between cancer-associated fibroblasts (CAFs) and neutrophils.
Akkermansia muciniphila alters host bile acid metabolism, increasing serum levels of tauroursodeoxycholic acid (TUDCA), which reduces PD-L1 expression on tumor cells and enhances T-cell infiltration
Akkermansia muciniphila works to repair the intestinal lining, which in turn reduces systemic lipopolysaccharide (LPS) and Bile acid metabolites. This process leads to a decrease in immunosuppressive myeloid-derived suppressor cells (MDSCs) and M2 macrophages.
During NSCLC treatment with Immune checkpoint inhibitors (ICIs), patients with higher baseline Akkermansia muciniphila abundance had better outcomes. They showed nearly double the objective response rate (41% vs. 19%). Their overall survival was longer (18.8 vs. 15.4 months). Akkermansia muciniphila was a better predictive biomarker than PD-L1 expression.
see also:
Akkermansia muciniphila & Immune Checkpoint Inhibitors (ICIs)
Anti-PD-1 antibodies / PD-1 inhibitors & Gut microbiota
Anti-PD-1 Antibodies / PD-1 Inhibitors & Non-Small-Cell-Lung-Cancer (NSCLC)
Biomarker & Immune checkpoint inhibitors (ICIs)
Chemokine (C-X-C motif) ligand 3 (CXCL3)-CD274 (Programmed death-ligand 1 (PD-L1)) axis
Fecal Microbiota Transplantation (FMT) (procedure-based) & Preclinical/Clinical data
Immune Checkpoint Inhibitors (ICIs) & Non-small-cell lung carcinoma (NSCLC)