Evidence map›Paper›PMID 33731830›Full record

ArticleMucosal immunology2021

Luminal microvesicles uniquely influence translocating bacteria after SIV infection.

Jacob K Flynn, Charlotte A Langner, Erik P Karmele, Phillip J Baker, Luxin Pei, Edlawit G Gorfu, Rachele M Bochart, Marianita Santiana, Margery G Smelkinson, Thomas B Nutman and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 40% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 1 country.

Jacob K Flynn *Barrier Immunity Section, Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA.
Charlotte A Langner *Barrier Immunity Section, Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA.
Erik P KarmeleMucosal Immunobiology Section, Laboratory of Molecular Immunology, NIAID, NIH, Bethesda, MD, USA.
Phillip J BakerBarrier Immunity Section, Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA.
Luxin PeiBarrier Immunity Section, Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA.
Edlawit G GorfuBarrier Immunity Section, Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA.
Rachele M BochartDivision of Animal Resources, Yerkes National Primate Research Center (YNPRC), Atlanta, GA, USA.
Marianita SantianaLaboratory of Host-Pathogen Dynamics, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Margery G SmelkinsonResearch Technologies Branch, NIAID, NIH, Bethesda, MD, USA.
Thomas B NutmanHelminth Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Nihal Altan-BonnetLaboratory of Host-Pathogen Dynamics, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Steven E BosingerYerkes Nonhuman Primate Genomics Core Laboratory, YNPRC, Atlanta, GA, USA.
Brian L KelsallMucosal Immunobiology Section, Laboratory of Molecular Immunology, NIAID, NIH, Bethesda, MD, USA.
Jason M BrenchleyBarrier Immunity Section, Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA. jbrenchl@niaid.nih.gov.
Alexandra M OrtizBarrier Immunity Section, Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA.
National Institutes of Health · USNational Institute of Allergy and Infectious Diseases · USAID Atlanta · USEmory National Primate Research CenterNational Heart Lung and Blood Institute · US

Funding

Infectious Diseases Research Technologies Core - BethesdaZICAI001051 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CHERRY, JAMES · 2009 to 2025
$226.1M
Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0M
Mechanisms of Immune Activation and Disease Progression in Animal ModelsZIAAI001029 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BRENCHLEY, JASON · 2009 to 2025
$28.2M
Antigen Processing And Presentation In The IntestineZIAAI000833 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KELSALL, BRIAN · 2009 to 2025
$24.9M
Immunoregulation /Immune Recognition In Filarial/Nonfilarial Parasitic InfectionZIAAI000197 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI NUTMAN, THOMAS · 2009 to 2025
$23.4M
Virus Egress PathwaysZIAHL006234 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ALTAN-BONNET, NIHAL · 2017 to 2025
$21.8M
Intramural NIH HHS ZIA AI001029NIH HHS P51 OD011132
6 · The paper itself

Abstract

Microbial translocation contributes to persistent inflammation in both treated and untreated HIV infection. Although translocation is due in part to a disintegration of the intestinal epithelial barrier, there is a bias towards the translocation of Proteobacteria. We hypothesized that intestinal epithelial microvesicle cargo differs after HIV infection and contributes to biased translocation. We isolated gastrointestinal luminal microvesicles before and after progressive simian immunodeficiency virus (SIV) infection in rhesus macaques and measured miRNA and antimicrobial peptide content. We demonstrate that these microvesicles display decreased miR-28-5p, -484, -584-3p, and -584-5p, and let-7b-3p, as well as increased beta-defensin 1 after SIV infection. We further observed dose-dependent growth sensitivity of commensal Lactobacillus salivarius upon co-culture with isolated microvesicles. Infection-associated microvesicle differences were not mirrored in non-progressively SIV-infected sooty mangabeys. Our findings describe novel alterations of antimicrobial control after progressive SIV infection that influence the growth of translocating bacterial taxa. These studies may lead to the development of novel therapeutics for treating chronic HIV infection, microbial translocation, and inflammation.

Indexed as

Bacterial TranslocationGastrointestinal MicrobiomeSimian Immunodeficiency VirusAnimalsBiomarkersDisease ProgressionDysbiosisExtracellular VesiclesIntestinal MucosaMacaca mulattaMicroRNAsSimian Acquired Immunodeficiency SyndromeBiomarkersMicroRNAs

Identifiers

PMID33731830
PMCPMC8225551
OpenAlexW3136159219

What OpenQuestion holds

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Registered trials

None linked

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 OpenQuestion graph.