Evidence map›Paper›PMID 28750066›Full record

ArticlePLoS pathogens2017

Cross-modulation of pathogen-specific pathways enhances malnutrition during enteric co-infection with Giardia lamblia and enteroaggregative Escherichia coli.

Luther A Bartelt, David T Bolick, Jordi Mayneris-Perxachs, Glynis L Kolling, Gregory L Medlock, Edna I Zaenker, Jeffery Donowitz, Rose Viguna Thomas-Beckett, Allison Rogala, Ian M Carroll and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
7.5field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 2 countries.

Luther A BarteltDivision of Infectious Diseases, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
David T BolickDivision of Infectious Diseases and International Health, Department of Medicine, University of Virginia, Charlottesville, Virginia, United States of America.
Jordi Mayneris-PerxachsDivision of Computational and Systems Medicine, Department of Surgery and Cancer, Imperial College London, United Kingdom.ORCID http://orcid.org/0000-0003-3788-3815
Glynis L KollingDivision of Infectious Diseases and International Health, Department of Medicine, University of Virginia, Charlottesville, Virginia, United States of America.ORCID http://orcid.org/0000-0001-8871-8129
Gregory L MedlockDepartment of Biomedical Engineering, University of Virginia, Charlottesville, Virginia, United States of America.ORCID http://orcid.org/0000-0002-1571-0801
Edna I ZaenkerDivision of Infectious Diseases and International Health, Department of Medicine, University of Virginia, Charlottesville, Virginia, United States of America.
Jeffery DonowitzDivision of Pediatric Infectious Diseases, Children's Hospital of Richmond at Virginia Commonwealth University, Richmond, Virginia, United States of America.
Rose Viguna Thomas-BeckettDivision of Infectious Diseases, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Allison RogalaCenter for Gastrointestinal Biology and Disease, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Ian M CarrollCenter for Gastrointestinal Biology and Disease, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Steven M SingerDepartment of Biology, Georgetown University, Washington, DC, United States of America.ORCID http://orcid.org/0000-0001-5719-7535
Jason PapinDepartment of Biomedical Engineering, University of Virginia, Charlottesville, Virginia, United States of America.ORCID http://orcid.org/0000-0002-2769-5805
Jonathan R SwannDivision of Computational and Systems Medicine, Department of Surgery and Cancer, Imperial College London, United Kingdom.
Richard L GuerrantDivision of Infectious Diseases and International Health, Department of Medicine, University of Virginia, Charlottesville, Virginia, United States of America.
University of Virginia · USUniversity of North Carolina at Chapel Hill · USImperial College London · GBGeorgetown University · USVirginia Commonwealth University · US

Funding

UNIV OF NORTH CAROLINA CLINICAL NUTRITION RESEARCH UNITP30DK056350 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Ian Michael Carroll · 1999 to 2026
$31.6M
PILOT AND FEASIBILITY STUDIESP30DK034987 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Temitope O. Keku · 1985 to 2026
$30.5M
Shigella Live Vector-Based Multivalent VaccineU19AI109776 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI LEVINE, MYRON MAX · 2014 to 2018
$25.4M
The Role of Macrophages in Immune Responses to GiardiaR15AI109591 · NIAID · GEORGETOWN UNIVERSITY · PI SINGER, STEVEN M · 2014 to 2023
$1.5M
Transdisciplinary Big Data Science Training at UVaT32LM012416 · NLM · UNIVERSITY OF VIRGINIA · PI BROWN, DONALD E, LOUGHRAN, THOMAS P. · 2016 to 2020
$1.3M
Cytokine signaling and IEC restitution in enteropathy: the Giardia paradigmK08AI108730 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BARTELT, LUTHER A · 2014 to 2018
$938k
NIAID NIH HHS K08 AI108730NIAID NIH HHS R15 AI109591NIAID NIH HHS U19 AI109776NIDDK NIH HHS P30 DK034987NIDDK NIH HHS P30 DK056350NLM NIH HHS T32 LM012416
6 · The paper itself

Abstract

Diverse enteropathogen exposures associate with childhood malnutrition. To elucidate mechanistic pathways whereby enteric microbes interact during malnutrition, we used protein deficiency in mice to develop a new model of co-enteropathogen enteropathy. Focusing on common enteropathogens in malnourished children, Giardia lamblia and enteroaggregative Escherichia coli (EAEC), we provide new insights into intersecting pathogen-specific mechanisms that enhance malnutrition. We show for the first time that during protein malnutrition, the intestinal microbiota permits persistent Giardia colonization and simultaneously contributes to growth impairment. Despite signals of intestinal injury, such as IL1α, Giardia-infected mice lack pro-inflammatory intestinal responses, similar to endemic pediatric Giardia infections. Rather, Giardia perturbs microbial host co-metabolites of proteolysis during growth impairment, whereas host nicotinamide utilization adaptations that correspond with growth recovery increase. EAEC promotes intestinal inflammation and markers of myeloid cell activation. During co-infection, intestinal inflammatory signaling and cellular recruitment responses to EAEC are preserved together with a Giardia-mediated diminishment in myeloid cell activation. Conversely, EAEC extinguishes markers of host energy expenditure regulatory responses to Giardia, as host metabolic adaptations appear exhausted. Integrating immunologic and metabolic profiles during co-pathogen infection and malnutrition, we develop a working mechanistic model of how cumulative diet-induced and pathogen-triggered microbial perturbations result in an increasingly wasted host.

Indexed as

AnimalsChildCoinfectionCytokinesDisease Models, AnimalEscherichia coliEscherichia coli InfectionsGiardia lambliaGiardiasisHumansIntestinal MucosaMaleMalnutritionMiceMice, Inbred C57BLMyeloid CellsCytokines

Identifiers

PMID28750066
PMCPMC5549954
OpenAlexW2740645471

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.