Bacterial toxin activation and deployment: Context-dependent links to host immune remodeling
4 affiliations
- 1Department of Clinical Laboratory, Affiliated Nanhua Hospital, Hengyang Medical College, University of South China, Hengyang, China
- 2Department of Clinical Laboratory, the Second Affiliated Hospital, Hengyang Medical College, University of South China, Hengyang, China
- 3Department of Blood Transfusion, the Second Affiliated Hospital, Hengyang Medical College, University of South China, Hengyang, China
- 4School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, Guangxi, China
Abstract
Many bacterial toxins are produced in latent or structurally constrained forms and acquire functional competence or productive access to host targets through distinct activation and deployment processes. This review distinguishes protein-level activation – including proteolytic maturation, reductive subunit release, metabolite-triggered autoprocessing, and host-factor-dependent catalytic activation – from receptor-mediated uptake, intracellular trafficking and translocation, vesicle-mediated delivery, and bacterial or phage-associated control of toxin expression and release. Across representative systems, these processes govern effector competence, availability, and localization and are associated with three broad immune outcomes: disruption of inflammatory signaling and cytokine networks, impairment of humoral defenses, and cell injury or regulated cell death. Their immune effects are often indirect and vary with host niche, cell type, receptor repertoire, trafficking route, and exposure timing. Distinguishing direct, effector-mediated, injury-mediated, availability-mediated, and unresolved relationships clarifies the boundaries of toxin activation and identifies priorities for in vivo validation and anti-virulence intervention.
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BibTeX
@article{xu2026bacterial,
title = {{Bacterial toxin activation and deployment: Context-dependent links to host immune remodeling}},
author = {Hao Xu and Chao Li and Xinchao Yi and Cheng Huang and Jinmei Zhang and Yuan Li and Ying Huang and Jing Chen and Jie Lu and Bin Liu and Jun He},
journal = {Virulence},
year = {2026},
month = oct,
doi = {10.1080/21505594.2026.2753301},
url = {https://doi.org/10.1080/21505594.2026.2753301},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Bacterial toxin activation and deployment: Context-dependent links to host immune remodeling
AU - Hao Xu
AU - Chao Li
AU - Xinchao Yi
AU - Cheng Huang
AU - Jinmei Zhang
AU - Yuan Li
AU - Ying Huang
AU - Jing Chen
AU - Jie Lu
AU - Bin Liu
AU - Jun He
PY - 2026
DA - 2026/10/29
JO - Virulence
DO - 10.1080/21505594.2026.2753301
UR - https://doi.org/10.1080/21505594.2026.2753301
AB - Many bacterial toxins are produced in latent or structurally constrained forms and acquire functional competence or productive access to host targets through distinct activation and deployment processes. This review distinguishes protein-level activation – including proteolytic maturation, reductive subunit release, metabolite-triggered autoprocessing, and host-factor-dependent catalytic activation – from receptor-mediated uptake, intracellular trafficking and translocation, vesicle-mediated delivery, and bacterial or phage-associated control of toxin expression and release. Across representative systems, these processes govern effector competence, availability, and localization and are associated with three broad immune outcomes: disruption of inflammatory signaling and cytokine networks, impairment of humoral defenses, and cell injury or regulated cell death. Their immune effects are often indirect and vary with host niche, cell type, receptor repertoire, trafficking route, and exposure timing. Distinguishing direct, effector-mediated, injury-mediated, availability-mediated, and unresolved relationships clarifies the boundaries of toxin activation and identifies priorities for in vivo validation and anti-virulence intervention.
SN - 2150-5594
SN - 2150-5608
ER -