Microbe-induced migrasome-like structures and their role in microbial persistence, immune evasion and transmission.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Microbe-induced migrasome-like structures and their role in microbial persistence, immune evasion and transmission.
Συγγραφείς: Feng M; Department of Infectious Diseases, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China; Department of Pathogen Biology, School of Clinical and Basic Medical Sciences, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China., Zhang L; Department of Infectious Diseases, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China; Department of Pathogen Biology, School of Clinical and Basic Medical Sciences, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China. Electronic address: armzhang@hotmail.com.
Πηγή: The Journal of infection [J Infect] 2026 Sep; Vol. 93 (3), pp. 106832. Date of Electronic Publication: 2026 Aug 18.
Τύπος έκδοσης: Journal Article; Review
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: W.B. Saunders Country of Publication: England NLM ID: 7908424 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1532-2742 (Electronic) Linking ISSN: 01634453 NLM ISO Abbreviation: J Infect Subsets: MEDLINE
Imprint Name(s): Publication: Kent, UK : W.B. Saunders
Original Publication: London, New York, Academic Press.
Ιατρικοί όροι (MeSH): Immune Evasion* , Host-Pathogen Interactions*, Mycoplasma/immunology ; Bacteria/immunology ; Humans ; Animals
Περίληψη: Microbial pathogens have evolved sophisticated strategies to disseminate within hosts, yet the full repertoire of intercellular transmission routes remains incompletely understood. Traditional models of microbial spread emphasize free-particle diffusion and direct cell-to-cell contact. Here, we extend our recently proposed "vimig" concept, originally confined to viruses, into a unifying framework of "microbe-induced migrasome-like structures" (mMig) that encompasses viruses, bacteria, and mycoplasmas. These migrasomes act as microbial Trojan horses, encapsulating intact pathogens together with host cellular debris. Functionally, mMig confers three cardinal pathogenic advantages: it enables receptor-independent entry into otherwise non-permissive cells; it supports non-lytic egress, allowing collective en bloc transmission while preserving host cell integrity; and it shields pathogens from immune attack and antimicrobial action, as mMig-encapsulated microbes resist antibody neutralization and antibiotic clearance. We examine how microbes exploit host factors to drive mMig biogenesis, and identify zinc ions as a natural dietary inhibitor of this pathway. Beyond dissemination, toxin-induced non-canonical migracytosis triggers rapid inflammatory responses, directly linking mMig to immunopathology. This review systematically catalogs ten viruses, large clostridial toxins (LCTs) produced by Clostridia, and Mycoplasma that induce mMig, compares three structural types (migrasome, retractosome, and migrion), and critically assesses host-directed interventions as potential broad-spectrum antimicrobial tools that could circumvent conventional resistance. Redefining these pathogen-induced vesicles as a conserved Achilles' heel in host-microbe interactions, we propose that targeted inhibition of mMig biogenesis offers a paradigm-shifting opportunity to combat refractory infections and alleviate infection-associated immunopathology.
(Copyright © 2026 The Authors. Published by Elsevier Ltd.. All rights reserved.)
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Contributed Indexing: Keywords: Host-pathogen interactions; Migrasome; Migrion; Vimig; mMig
Entry Date(s): Date Created: 20260818 Date Completed: 20260928 Latest Revision: 20260928
Update Code: 20260929
DOI: 10.1016/j.jinf.2026.106832
PMID: 42612734
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1532-2742
DOI:10.1016/j.jinf.2026.106832