Evidence map›Paper›PMID 25348635›Full record

ArticleInfection and immunity2015

Intestinal alkaline phosphatase deficiency leads to lipopolysaccharide desensitization and faster weight gain.

Ye Yang, José Luis Millán, Joan Mecsas, Karen Guillemin

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  8. Marine Microalgae,Marine drugs · 2020
    Article
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  11. 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

4 authors at 3 institutions in 1 country.

Ye YangInstitute of Molecular Biology, University of Oregon, Eugene, Oregon, USA.
José Luis MillánSanford Children's Health Research Center, Sanford-Burnham Medical Research Institute, La Jolla, California, USA.
Joan MecsasDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, and Graduate Program in Molecular Microbiology, Sackler School of Biomedical Sciences, Boston, Massachusetts, USA.
Karen GuilleminInstitute of Molecular Biology, University of Oregon, Eugene, Oregon, USA guillemin@molbio.uoregon.edu.
University of Oregon · USSanford Burnham Prebys Medical Discovery Institute · USTufts University · US

Funding

Research Area IIIP50GM098911 · NIGMS · UNIVERSITY OF OREGON · PI PARTHASARATHY, RAGHUVEER · 2012 to 2016
$9.8M
Molecular basis of host-microbiota signaling in the zebrafish gutR01DK075549 · NIDDK · UNIVERSITY OF OREGON · PI GUILLEMIN, KAREN J · 2007 to 2011
$1.8M
NIDDK NIH HHS R01 DK075549NIDDK NIH HHS R01DK075549NIGMS NIH HHS P50 GM098911NIGMS NIH HHS P50GM098911
6 · The paper itself

Abstract

Animals develop in the presence of complex microbial communities, and early host responses to these microbes can influence key aspects of development, such as maturation of the immune system, in ways that impact adult physiology. We previously showed that the zebrafish intestinal alkaline phosphatase (ALPI) gene alpi.1 was induced by Gram-negative bacterium-derived lipopolysaccharide (LPS), a process dependent on myeloid differentiation primary response gene 88 (MYD88), and functioned to detoxify LPS and prevent excessive host inflammatory responses to commensal microbiota in the newly colonized intestine. In the present study, we examined whether the regulation and function of ALPI were conserved in mammals. We found that among the mouse ALPI genes, Akp3 was specifically upregulated by the microbiota, but through a mechanism independent of LPS or MYD88. We showed that disruption of Akp3 did not significantly affect intestinal inflammatory responses to commensal microbiota or animal susceptibility to Yersinia pseudotuberculosis infection. However, we found that Akp3(-/-) mice acquired LPS tolerance during postweaning development, suggesting that Akp3 plays an important role in immune education. Finally, we demonstrated that inhibiting LPS sensing with a mutation in CD14 abrogated the accelerated weight gain in Akp3(-/-) mice receiving a high-fat diet, suggesting that the weight gain is caused by excessive LPS in Akp3(-/-) mice.

Indexed as

Immune ToleranceAlkaline PhosphataseAnimalsFemaleGram-Negative BacteriaIntestinesLipopolysaccharidesMaleMice, Inbred C57BLMice, KnockoutWeight GainAkp3 protein, mouseAlkaline PhosphataseLipopolysaccharides

Identifiers

PMID25348635
PMCPMC4288875
OpenAlexW2020938662

What OpenQuestion holds

Textmetadata
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.