Evidence map›Paper›PMID 26259151›Full record

ArticleNature communications2015

Oestrogen sulfotransferase ablation sensitizes mice to sepsis.

Xiaojuan Chai, Yan Guo, Mengxi Jiang, Bingfang Hu, Zhigang Li, Jie Fan, Meihong Deng, Timothy R Billiar, Heidi R Kucera, Nilesh W Gaikwad and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  4. N-acetyltransferase 10 mediates cognitive dysfunction through the acetylation of GABAProceedings of the National Academy of Sciences of the United States of America · 2024
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  8. Xenobiotic Receptors, a Journey of Rewards.Drug metabolism and disposition: the biological fate of chemicals · 2023
    Review
  9. Sex differences in cardiovascular response to sepsis.American journal of physiology. Cell physiology · 2023
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. The Role of Sulfotransferases in Liver Diseases.Drug metabolism and disposition: the biological fate of chemicals · 2020
    Review
  15. Inhibition of Estrogen Sulfotransferase (Journal of the American Society of Nephrology : JASN · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

19 authors at 5 institutions in 2 countries.

Xiaojuan Chai1] Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA [2] Department of Pharmaceutical Analysis and Drug Metabolism, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China.
Yan Guo1] Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA [2] Department of Pathology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Mengxi JiangCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Bingfang Hu1] Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA [2] Institute of Clinical Pharmacology, Sun Yat-Sen University, Guangzhou, Guangdong 510006, China.
Zhigang LiSurgical Research, Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, Pennsylvania 15240, USA.
Jie Fan1] Surgical Research, Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, Pennsylvania 15240, USA [2] Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Meihong DengDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Timothy R BilliarDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Heidi R KuceraDepartment of Nutrition and Department of Environmental Toxicology, University of California, Davis, California 95616, USA.
Nilesh W GaikwadDepartment of Nutrition and Department of Environmental Toxicology, University of California, Davis, California 95616, USA.
Meishu XuCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Peipei LuCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Jiong YanCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Haiyan FuDepartment of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Youhua LiuDepartment of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Lushan Yu1] Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA [2] Department of Pharmaceutical Analysis and Drug Metabolism, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China.
Min HuangInstitute of Clinical Pharmacology, Sun Yat-Sen University, Guangzhou, Guangdong 510006, China.
Su ZengDepartment of Pharmaceutical Analysis and Drug Metabolism, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China.
Wen Xie1] Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA [2] Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
University of Pittsburgh · USUniversity of California, Davis · USVA Pittsburgh Healthcare System · USZhejiang University · CNSun Yat-sen University · CN

Funding

Regulation of Intestinal Mucosal Injury & Repair After Trauma/Hemorrhagic ShockP50GM053789 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI VODOVOTZ, YORAM · 1997 to 2013
$18.0M
Regulation and Function of Endotoxin Signaling in Surgical SepsisR01GM050441 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BILLIAR, TIMOTHY R · 1994 to 2018
$4.6M
Cell Priming, Receptor Cross-Talk, and Acute Lung InjuryR01HL079669 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FAN, JIE, WILSON, MARK A. · 2005 to 2019
$4.0M
NITRIC OXIDE AND HEPATIC FUNCTION IN SEPSIS AND TRAUMAR01GM044100 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BILLIAR, TIMOTHY R · 1995 to 2017
$1.9M
A Novel Regulation of the Phase II Enzyme Estrogen SulfotransferaseR01ES023438 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIE, WEN · 2014 to 2018
$1.7M
The Perinatal Pharmacology of the Nuclear ReceptorR01HD073070 · NICHD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIE, WEN · 2013 to 2017
$1.6M
The hepatic function of cholesterol sulfotransferase 2B1b (SULT2B1b)in energy metR01DK099232 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIE, WEN · 2014 to 2017
$1.3M
NHLBI NIH HHS R01 HL079669NICHD NIH HHS R01 HD073070NIEHS NIH HHS R01 ES023438NIGMS NIH HHS P50 GM053789NIGMS NIH HHS R01 GM044100NIGMS NIH HHS R01 GM050441
6 · The paper itself

Abstract

Sepsis is the host's deleterious systemic inflammatory response to microbial infections. Here we report an essential role for the oestrogen sulfotransferase (EST or SULT1E1), a conjugating enzyme that sulfonates and deactivates estrogens, in sepsis response. Both the caecal ligation and puncture (CLP) and lipopolysaccharide models of sepsis induce the expression of EST and compromise the activity of oestrogen, an anti-inflammatory hormone. Surprisingly, EST ablation sensitizes mice to sepsis-induced death. Mechanistically, EST ablation attenuates sepsis-induced inflammatory responses due to compromised oestrogen deactivation, leading to increased sepsis lethality. In contrast, transgenic overexpression of EST promotes oestrogen deactivation and sensitizes mice to CLP-induced inflammatory response. The induction of EST by sepsis is NF-κB dependent and EST is a NF-κB-target gene. The reciprocal regulation of inflammation and EST may represent a yet-to-be-explored mechanism of endocrine regulation of inflammation, which has an impact on the clinical outcome of sepsis.

Indexed as

AnimalsCecumEstrogensFemaleGenetic Predisposition to DiseaseHep G2 CellsHumansKupffer CellsLiverMiceMice, KnockoutSepsisSulfotransferasesToll-Like Receptor 4UterusEstrogensestrone sulfotransferaseSulfotransferasesTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID26259151
PMCPMC4532951
OpenAlexW2255369262

What OpenQuestion holds

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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.