Evidence map›Paper›PMID 26146866›Full record

ArticleMicrobiology and immunology2015

Escherichia coli heme oxygenase modulates host innate immune responses.

Nitsan Maharshak, Hyungjin Sally Ryu, Ting-Jia Fan, Joseph C Onyiah, Stephanie Schulz, Sherrie L Otterbein, Ron Wong, Jonathan J Hansen, Leo E Otterbein, Ian M Carroll and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Microbiology and immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
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  9. The role of gasotransmitters in neonatal physiology.Nitric oxide : biology and chemistry · 2020
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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

11 authors at 4 institutions in 2 countries.

Nitsan MaharshakDepartment of Medicine and Center for GI Biology and Diseases, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, 27599.
Hyungjin Sally RyuDepartment of Medicine and Center for GI Biology and Diseases, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, 27599.
Ting-Jia FanDepartment of Medicine and Center for GI Biology and Diseases, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, 27599.
Joseph C OnyiahDepartment of Medicine and Center for GI Biology and Diseases, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, 27599.
Stephanie SchulzDepartment of Pediatrics, Division of Neonatal and Developmental Medicine, Stanford University School of Medicine, Palo Alto, California, 94305.
Sherrie L OtterbeinDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, 02115, USA.
Ron WongDepartment of Pediatrics, Division of Neonatal and Developmental Medicine, Stanford University School of Medicine, Palo Alto, California, 94305.
Jonathan J HansenDepartment of Medicine and Center for GI Biology and Diseases, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, 27599.
Leo E OtterbeinDepartment of Pediatrics, Division of Neonatal and Developmental Medicine, Stanford University School of Medicine, Palo Alto, California, 94305.
Ian M CarrollDepartment of Medicine and Center for GI Biology and Diseases, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, 27599.
Scott E PlevyDepartment of Medicine and Center for GI Biology and Diseases, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, 27599.
University of North Carolina at Chapel Hill · USStanford University · USDenver VA Medical Center · USHarvard University · US

Funding

PILOT AND FEASIBILITY STUDIESP30DK034987 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ROBERT S. SANDLER · 1985 to 2026
$30.5M
GASTROENTEROLOGY RESEARCH TRAININGT32DK007737 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SHEHZAD Z. SHEIKH · 1996 to 2026
$7.8M
MACROPHAGE GENE EXPRESSION IN MUCOSAL INFLAMMATIONR01DK054452 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PLEVY, SCOTT E · 2000 to 2010
$2.6M
Medical Student Scholars Program at UNC NIDDK CentersT32DK062666 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SANDLER, ROBERT S. · 2002 to 2006
$262k
NIDDK NIH HHS P30 DK034987NIDDK NIH HHS R01 DK054452NIDDK NIH HHS R01 DK54452NIDDK NIH HHS T32 DK007737NIDDK NIH HHS T32 DK062666
6 · The paper itself

Abstract

Induction of mammalian heme oxygenase (HO)-1 and exposure of animals to carbon monoxide (CO) ameliorates experimental colitis. When enteric bacteria, including Escherichia coli, are exposed to low iron conditions, they express an HO-like enzyme, chuS, and metabolize heme into iron, biliverdin and CO. Given the abundance of enteric bacteria residing in the intestinal lumen, our postulate was that commensal intestinal bacteria may be a significant source of CO and those that express chuS and other Ho-like molecules suppress inflammatory immune responses through release of CO. According to real-time PCR, exposure of mice to CO results in changes in enteric bacterial composition and increases E. coli 16S and chuS DNA. Moreover, the severity of experimental colitis correlates positively with E. coli chuS expression in IL-10 deficient mice. To explore functional roles, E. coli were genetically modified to overexpress chuS or the chuS gene was deleted. Co-culture of chuS-overexpressing E. coli with bone marrow-derived macrophages resulted in less IL-12p40 and greater IL-10 secretion than in wild-type or chuS-deficient E. coli. Mice infected with chuS-overexpressing E. coli have more hepatic CO and less serum IL-12 p40 than mice infected with chuS-deficient E. coli. Thus, CO alters the composition of the commensal intestinal microbiota and expands populations of E. coli that harbor the chuS gene. These bacteria are capable of attenuating innate immune responses through expression of chuS. Bacterial HO-like molecules and bacteria-derived CO may represent novel targets for therapeutic intervention in inflammatory conditions.

Indexed as

Immune EvasionImmunity, InnateAnimalsCarbon MonoxideCells, CulturedCoculture TechniquesDNA, BacterialDNA, RibosomalEscherichia coliGene DeletionGene ExpressionHeme Oxygenase (Decyclizing)Interleukin-10Interleukin-12 Subunit p40MacrophagesMaleCarbon MonoxideDNA, BacterialDNA, RibosomalHeme Oxygenase (Decyclizing)Interleukin-10Interleukin-12 Subunit p40RNA, Ribosomal, 16Scarbon monoxidechuSenteric microbiotaheme oxygenase

Identifiers

PMID26146866
PMCPMC4582649
OpenAlexW1933800203

What OpenQuestion holds

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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.