Evidence map›Paper›PMID 26376368›Full record

ArticleMucosal immunology2016

Gut immune dysfunction through impaired innate pattern recognition receptor expression and gut microbiota dysbiosis in chronic SIV infection.

T W Glavan, C A Gaulke, C Santos Rocha, S Sankaran-Walters, L A Hirao, M Raffatellu, G Jiang, A J Bäumler, L R Goulart, S Dandekar

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 64 citations in OpenAlex.

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  13. Microbiome Studies in Non-human Primates.Current HIV/AIDS reports · 2021
    Review
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  16. Article
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  20. The gut microbiome and frailty.Translational research : the journal of laboratory and clinical medicine · 2020
    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

10 authors at 2 institutions in 2 countries.

T W GlavanDepartment of Medical Microbiology and Immunology, University of California, Davis, California, USA.
C A GaulkeDepartment of Medical Microbiology and Immunology, University of California, Davis, California, USA.
C Santos RochaDepartment of Medical Microbiology and Immunology, University of California, Davis, California, USA.
S Sankaran-WaltersDepartment of Medical Microbiology and Immunology, University of California, Davis, California, USA.
L A HiraoDepartment of Medical Microbiology and Immunology, University of California, Davis, California, USA.
M RaffatelluDepartment of Microbiology and Molecular Genetics, University of California, Irvine, California, USA.
G JiangDepartment of Medical Microbiology and Immunology, University of California, Davis, California, USA.
A J BäumlerDepartment of Medical Microbiology and Immunology, University of California, Davis, California, USA.
L R GoulartDepartment of Medical Microbiology and Immunology, University of California, Davis, California, USA.
S DandekarDepartment of Medical Microbiology and Immunology, University of California, Davis, California, USA.
University of California Davis Medical Center · USUniversity of California, Irvine · US

Funding

National Institute on Aging (NIA) ColonyP51OD011107 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Simon J. Atkinson · 2012 to 2026
$191.5M
INTESTINAL CYTOKINE &TCELL HOMEOSTASIS IN SIV INFECTIONR01AI043274 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI DANDEKAR, SATYA · 1998 to 2013
$5.1M
HIV reservoir and CD4 repopulation in gut lymphoid tissueR01DK061297 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI DANDEKAR, SATYA · 2002 to 2012
$3.5M
NIAID NIH HHS R01 AI043274NIDDK NIH HHS R01 DK061297NIH HHS P51 OD011107
6 · The paper itself

Abstract

HIV targets the gut mucosa early in infection, causing immune and epithelial barrier dysfunction and disease progression. However, gut mucosal sensing and innate immune signaling through mucosal pattern recognition receptors (PRRs) during HIV infection and disease progression are not well defined. Using the simian immunodeficiency virus (SIV)-infected rhesus macaque model of AIDS, we found a robust increase in PRRs and inflammatory cytokine gene expression during the acute SIV infection in both peripheral blood and gut mucosa, coinciding with viral replication. PRR expression remained elevated in peripheral blood following the transition to chronic SIV infection. In contrast, massive dampening of PRR expression was detected in the gut mucosa, despite the presence of detectable viral loads. Exceptionally, expression of Toll-like receptor 4 (TLR4) and TLR8 was downmodulated and diverged from expression patterns for most other TLRs in the gut. Decreased mucosal PRR expression was associated with increased abundance of several pathogenic bacterial taxa, including Pasteurellaceae members, Aggregatibacter and Actinobacillus, and Mycoplasmataceae family. Early antiretroviral therapy led to viral suppression but only partial maintenance of gut PRRs and cytokine gene expression. In summary, SIV infection dampens mucosal innate immunity through PRR dysregulation and may promote immune activation, gut microbiota changes, and ineffective viral clearance.

Indexed as

AnimalsChronic DiseaseDysbiosisGastrointestinal MicrobiomeGene Expression RegulationHIV InfectionsHumansImmune EvasionImmunity, MucosalMacaca mulattaReceptors, Pattern RecognitionSignal TransductionSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusToll-Like Receptor 4Toll-Like Receptor 8Receptors, Pattern RecognitionToll-Like Receptor 4Toll-Like Receptor 8

Identifiers

PMID26376368
PMCPMC4794436
OpenAlexW2215507423

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.