This study investigated how chronic stress-induced gut microbiota disruption affects anti-tumor immunity, using mouse models of colorectal cancer and melanoma, and extending findings to human cancer samples.
Chronic stress promotes translocation of gut pathobiont *Enterococcus gallinarum* (Eg) to tumors; intratumoral Eg phage DNA drives glucocorticoid production by cancer-associated fibroblasts (CAFs) via TLR9, suppressing anti-tumor germinal center B cell responses. Targeting intratumoral TLR9 or Eg lowered intratumor glucocorticoid levels and reversed tumor-promoting effects of stress. Lytic phages from a *Klebsiella pneumoniae* isolate in human colorectal tumors also promoted tumor growth, and phage DNA was detected in human brain tumors.
Full text was inaccessible; key quantitative outcomes (effect sizes, sample sizes, p-values) cannot be confirmed. Findings are largely preclinical (mouse models), with human data limited to translational observations rather than interventional studies.
This research is preclinical; direct clinical application is not yet established. However, clinicians should be aware that chronic psychological stress may impair anti-tumor immunity via a gut microbiome–intratumoral phage–CAF–B cell axis, suggesting future therapeutic targets in intratumoral TLR9 signaling or pathobiont reduction.
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