ReviewFrontiers in microbiology2026
Type VI secretion system effectors as modulators of host immunometabolism: organelle stress, nutritional immunity, and therapeutic opportunities.
Review in Frontiers in microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Metabolic reprogramming is a central determinant of host defense and pathogen persistence during infection. Although the bacterial type VI secretion system (T6SS) is primarily recognized as a contact-dependent apparatus for interbacterial competition and effector delivery, emerging evidence indicates that T6SS activity can also influence host metabolism at cellular, nutritional, and microbial-community levels. Here, we organize current evidence into three mechanistic tiers: direct biochemical interference with lipids, metabolites, or metal ions; organelle- and signaling-mediated immunometabolic reprogramming; and indirect metabolic effects arising from T6SS-dependent remodeling of microbial communities. T6SS effectors can disrupt endoplasmic-reticulum lipid homeostasis, activate the unfolded protein response and autophagy, alter mitochondrial Ca2+ handling and dynamics, promote redox imbalance, and modulate metabolically sensitive immune pathways including phosphoinositide 3-kinase (PI3K)-Akt, inflammasome, and cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling. T6SS-associated proteins also mediate manganese and zinc acquisition or sequestration, linking microbial nutrient acquisition to host nutritional immunity. At the community level, T6SS-mediated competition may reshape resource allocation, horizontal gene transfer, and microbiome-derived metabolite production. However, while T6SS-induced organelle stress is well established, direct causal links to systemic metabolic diseases, including type 2 diabetes and dyslipidemia, remain unproven. We therefore distinguish direct metabolic measurements from inferences based on organelle damage or signaling changes and discuss strategies to define T6SS-driven metabolic fluxes and evaluate host-directed, anti-virulence, and microbiome-engineering approaches. Viewing the T6SS through an immunometabolic framework may reveal therapeutic vulnerabilities overlooked by conventional models of bacterial toxicity and competition.
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