ArticlemBio2022
The Obligate Intracellular Bacterial Pathogen Anaplasma phagocytophilum Exploits Host Cell Multivesicular Body Biogenesis for Proliferation and Dissemination.
Article in mBio, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Machine Learning-Based Detection ofPathogens (Basel, Switzerland) · 2026Article
- Obligatory intracellular bacterium Anaplasma phagocytophilum AnkA regulates actin dynamics and spatiotemporal bacterial release.PLoS pathogens · 2026Article
- The Outcome of Intracellular Selenomonas sputigena and its Impact on Gingival Keratinocytes.Molecular oral microbiology · 2026Article
- Whole transcriptome analysis reveals differential gene expression associated with Anaplasma phagocytophilum invading HL-60 cells.Parasites & vectors · 2026Article
- Article
- Classification and biogenesis of vesicles, and their roles in the transport of viral components.Archives of microbiology · 2026Review
- Distinct modes of cell division drivemBio · 2025Article
- Nexinhib20 inhibits JFC1-mediated mobilization of a subset of CD11b/CD18+ vesicles decreasing integrin avidity, but does not inhibit Rac1.Journal of leukocyte biology · 2025Article
- Exosomes in Diabetic Wound Healing: Mechanisms, Applications, and Perspectives.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Article
- The multifunctionProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- The role of Rab27 in tick extracellular vesicle biogenesis and pathogen infection.Parasites & vectors · 2024Article
- Microsporidia persistence in host impairs epithelial barriers and increases chances of inflammatory bowel disease.Microbiology spectrum · 2024Article
- A glimpse into the world of microRNAs and their putative roles in hard ticks.Frontiers in cell and developmental biology · 2024Review
- Rab27 in tick extracellular vesicle biogenesis and infection.bioRxiv : the preprint server for biology · 2023Article
- Tick extracellular vesicles in host skin immunity and pathogen transmission.Trends in parasitology · 2023Review
- The multifaceted interactions between pathogens and host ESCRT machinery.PLoS pathogens · 2023Review
- Innate immunity in rickettsial infections.Frontiers in cellular and infection microbiology · 2023Review
- Establishing the intracellular niche of obligate intracellular vacuolar pathogens.Frontiers in cellular and infection microbiology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Anaplasma phagocytophilum is the etiologic agent of the emerging infection, granulocytic anaplasmosis. This obligate intracellular bacterium lives in a host cell-derived vacuole that receives membrane traffic from multiple organelles to fuel its proliferation and from which it must ultimately exit to disseminate infection. Understanding of these essential pathogenic mechanisms has remained poor. Multivesicular bodies (MVBs) are late endosomal compartments that receive biomolecules from other organelles and encapsulate them into intralumenal vesicles (ILVs) using endosomal sorting complexes required for transport (ESCRT) machinery and ESCRT-independent machinery. Association of the ESCRT-independent protein, ALIX, directs MVBs to the plasma membrane where they release ILVs as exosomes. We report that the A. phagocytophilum vacuole (ApV) is acidified and enriched in lysobisphosphatidic acid, a lipid that is abundant in MVBs. ESCRT-0 and ESCRT-III components along with ALIX localize to the ApV membrane. siRNA-mediated inactivation of ESCRT-0 and ALIX together impairs A. phagocytophilum proliferation and infectious progeny production. RNA silencing of ESCRT-III, which regulates ILV scission, pronouncedly reduces ILV formation in ApVs and halts infection by arresting bacterial growth. Rab27a and its effector Munc13-4, which drive MVB trafficking to the plasma membrane and subsequent exosome release, localize to the ApV. Treatment with Nexinhib20, a small molecule inhibitor that specifically targets Rab27a to block MVB exocytosis, abrogates A. phagocytophilum infectious progeny release. Thus, A. phagocytophilum exploits MVB biogenesis and exosome release to benefit each major stage of its intracellular infection cycle: intravacuolar growth, conversion to the infectious form, and exit from the host cell.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.