bims-migras 2026-08-23 papers

Issue of 2026–08–23
two papers selected by
Cliff Dominy

J Biosci Bioeng. 2026 Aug 22. pii: S1389-1723(26)00249-5. [Epub ahead of print]

Proteomic analysis of migrasomes derived from IL-6 amplifier-induced human breast cancer cells.

Ananda Bagus Richky Digdaya Putra, Shogo Saito, Yuka Iwasaki, Masayoshi Tanaka, Mina Okochi.

Migrasomes are extracellular vesicles secreted by migrating cells that mediate intercellular communication and contribute to inflammation and cancer progression. We have previously demonstrated that IL-6 expression is induced in cells that have taken up migrasomes derived from IL-6 amplifier activated cells, suggesting that migrasomes are involved in the propagation of inflammation. However, the molecular changes occurring within migrasomes upon IL-6 amplifier remain unknown. In this study, migrasome-enriched samples were extracted from IL-6 amplification-induced human breast cancer MDA-MB-231 cells by ultracentrifugation, and comparative proteomics analysis was performed. Shotgun proteomics detected a total of 1984 proteins, of which 1339 were detected under all conditions. In the cytokine-stimulated migrasomes, 330 proteins up-regulated and 149 proteins down-regulated compared to starvation condition. Changes associated with IL-6 amplification included the IL-6 pathway kinase JAK1, proteins involved in vesicular transport, and SNARE family members syntaxin-3 and syntaxin-4. After immunostaining, the fluorescence of JAK1 in migrasomes under stimulation condition was approximately 1.5-fold higher than those under starvation condition, consistent with the proteomic result. Furthermore, functional enrichment analysis revealed enhanced expression of pathways related to oxidative phosphorylation, endoplasmic reticulum protein processing, and cell organization. These findings indicate that IL-6 amplifier activation is associated with coordinated changes in migrasome proteins, including those involved in inflammatory signaling and trafficking. This study provides a proteomic understanding of migrasome-mediated inflammatory communication in the tumor microenvironment.

Keywords: Cytokines; IL-6 amplifier; Inflammation; Migrasome; Proteomics

DOI: https://doi.org/10.1016/j.jbiosc.2026.08.001

J Infect. 2026 Aug 18. pii: S0163-4453(26)00158-1. [Epub ahead of print] 106832

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

Mingyan Feng, Leiliang Zhang.

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.

Keywords: host-pathogen interactions; mMig; migrasome; migrion; vimig

DOI: https://doi.org/10.1016/j.jinf.2026.106832