Evidence map›Paper›PMID 32859011›Full record

ArticleToxins2020

Germ-Free Conditions Modulate Host Purine Metabolism, Exacerbating Adenine-Induced Kidney Damage.

Eikan Mishima, Mariko Ichijo, Takeshi Kawabe, Koichi Kikuchi, Yukako Akiyama, Takafumi Toyohara, Takehiro Suzuki, Chitose Suzuki, Atsuko Asao, Naoto Ishii and 2 more

Open access · goldAbstract read
In one paragraph

Article in Toxins, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. DRIVERS OF VARIATION OF THE ZEBRAFISH EGG MICROBIOME.bioRxiv : the preprint server for biology · 2025
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Monkfish (Molecules (Basel, Switzerland) · 2022
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Role of the microbiota in hypertension and antihypertensive drug metabolism.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. 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

12 authors at 2 institutions in 1 country.

Eikan MishimaDivision of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.ORCID 0000-0002-3706-2745
Mariko IchijoDivision of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Takeshi KawabeDepartment of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Koichi KikuchiDivision of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Yukako AkiyamaDivision of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Takafumi ToyoharaDivision of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.ORCID 0000-0001-7655-3005
Takehiro SuzukiDivision of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Chitose SuzukiDivision of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Atsuko AsaoDepartment of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Naoto IshiiDepartment of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Shinji FukudaInstitute for Advanced Biosciences, Keio University, Tsuruoka 997-0052, Japan.ORCID 0000-0001-5161-9880
Takaaki AbeDivision of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Tohoku University · JPUniversity of Tsukuba · JP

Funding

Core Research for Evolutional Science and Technology JP19gm1010009Exploratory Research for Advanced Technology JPMJER1902Food Science Institute Foundation S.F.HIROMI Medical Research Foundation E.M.Japan Foundation for Applied Enzymology E.M.Japan Society for the Promotion of Science London 18K08198Okinaka Memorial Institute for Medical Research Grant E.M.Program for the Advancement of Research in Core Projects under Keio University's Longevity Initiative S.F.Takeda Science Foundation S.F.The Japan Health Foundation E.M.Tohoku University Center for Gender Equality Promotion (TUMUG) Support Project E.M.
6 · The paper itself

Abstract

Alterations in microbiota are known to affect kidney disease conditions. We have previously shown that germ-free conditions exacerbated adenine-induced kidney damage in mice; however, the mechanism by which this occurs has not been elucidated. To explore this mechanism, we examined the influence of germ-free conditions on purine metabolism and renal immune responses involved in the kidney damage. Germ-free mice showed higher expression levels of purine-metabolizing enzymes such as xanthine dehydrogenase, which converts adenine to a nephrotoxic byproduct 2,8-dihydroxyadenine (2,8-DHA). The germ-free mice also showed increased urinary excretion of allantoin, indicating enhanced purine metabolism. Metabolome analysis demonstrated marked differences in the purine metabolite levels in the feces of germ-free mice and mice with microbiota. Furthermore, unlike the germ-free condition, antibiotic treatment did not increase the expression of purine-metabolizing enzymes or exacerbate adenine-induced kidney damage. Considering renal immune responses, the germ-free mice displayed an absence of renal IL-17A expression. However, the adenine-induced kidney damage in wild-type mice was comparable to that in IL-17A-deficient mice, suggesting that IL-17A does not play a major role in the disease condition. Our results suggest that the enhanced host purine metabolism in the germ-free mice potentially promotes the conversion of the administered adenine into 2,8-DHA, resulting in exacerbated kidney damage. This further suggests a role of the microbiota in regulating host purine metabolism.

Indexed as

Acute Kidney InjuryAdenineAnimalsGerm-Free LifeInterleukin-17MaleMiceMice, Inbred C57BLMice, TransgenicPurinesAdenineIl17a protein, mouseInterleukin-17Purineschronic kidney diseasegut-kidney axisIL-17microbiotaTh17uremic toxinsuric acidsxanthine dehydrogenasexanthine oxidase

Identifiers

PMID32859011
PMCPMC7551802
OpenAlexW3080574910

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.