Evidence map›Paper›PMID 26726767›Full record

ArticlePLoS genetics2016

TrpA1 Regulates Defecation of Food-Borne Pathogens under the Control of the Duox Pathway.

Eun Jo Du, Tae Jung Ahn, Ilmin Kwon, Ji Hye Lee, Jeong-Ho Park, Sun Hwa Park, Tong Mook Kang, Hana Cho, Tae Jin Kim, Hyung-Wook Kim and 5 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 84 citations in OpenAlex.

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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

15 authors at 6 institutions in 1 country.

Eun Jo DuSamsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Korea.
Tae Jung AhnSamsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Korea.
Ilmin KwonSamsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Korea.
Ji Hye LeeSamsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Korea.
Jeong-Ho ParkDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Korea.
Sun Hwa ParkSamsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Korea.
Tong Mook KangSamsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Korea.
Hana ChoSamsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Korea.
Tae Jin KimSamsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Korea.
Hyung-Wook KimCollege of Life Sciences, Sejong University, Seoul, Korea.
Youngsoo JunSchool of Life Sciences, Gwangju Institute of Science and Technology (GIST), Gwangju, Korea.
Hee Jae LeeKangwon National University College of Medicine, Chuncheon, Korea.
Young Sik LeeCollege of Life Sciences and Biotechnology, Korea University, Seoul, Korea.
Jae Young KwonDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Korea.
KyeongJin KangSamsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Korea.
Samsung (South Korea) · KRSungkyunkwan University · KRGwangju Institute of Science and Technology · KRKangwon National University · KRKorea University · KRSejong University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathogen expulsion from the gut is an important defense strategy against infection, but little is known about how interaction between the intestinal microbiome and host immunity modulates defecation. In Drosophila melanogaster, dual oxidase (Duox) kills pathogenic microbes by generating the microbicidal reactive oxygen species (ROS), hypochlorous acid (HOCl) in response to bacterially excreted uracil. The physiological function of enzymatically generated HOCl in the gut is, however, unknown aside from its anti-microbial activity. Drosophila TRPA1 is an evolutionarily conserved receptor for reactive chemicals like HOCl, but a role for this molecule in mediating responses to gut microbial content has not been described. Here we identify a molecular mechanism through which bacteria-produced uracil facilitates pathogen-clearing defecation. Ingestion of uracil increases defecation frequency, requiring the Duox pathway and TrpA1. The TrpA1(A) transcript spliced with exon10b (TrpA1(A)10b) that is present in a subset of midgut enteroendocrine cells (EECs) is critical for uracil-dependent defecation. TRPA1(A)10b heterologously expressed in Xenopus oocytes is an excellent HOCl receptor characterized with elevated sensitivity and fast activation kinetics of macroscopic HOCl-evoked currents compared to those of the alternative TRPA1(A)10a isoform. Consistent with TrpA1's role in defecation, uracil-excreting Erwinia carotovora showed higher persistence in TrpA1-deficient guts. Taken together, our results propose that the uracil/Duox pathway promotes bacteria expulsion from the gut through the HOCl-sensitive receptor, TRPA1(A)10b, thereby minimizing the chances that bacteria adapt to survive host defense systems.

Indexed as

AnimalsBacteriaDrosophila melanogasterDrosophila ProteinsFoodborne DiseasesGene Expression RegulationHost-Pathogen InteractionsHumansHypochlorous AcidIon ChannelsNADPH OxidasesOocytesReactive Oxygen SpeciesTRPA1 Cation ChannelTRPC Cation ChannelsXenopusDrosophila Proteinsdual oxidase, DrosophilaHypochlorous AcidIon ChannelsNADPH OxidasesReactive Oxygen SpeciesTRPA1 Cation ChannelTrpA1 protein, DrosophilaTRPC Cation Channels

Identifiers

PMID26726767
PMCPMC4699737
OpenAlexW2229779164

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.