Evidence map›Paper›PMID 27145012›Full record

ArticleEndocrinology2016

11β-Hydroxysteroid Dehydrogenase Type 1 Is Expressed in Neutrophils and Restrains an Inflammatory Response in Male Mice.

Agnes E Coutinho, Tiina M J Kipari, Zhenguang Zhang, Cristina L Esteves, Christopher D Lucas, James S Gilmour, Scott P Webster, Brian R Walker, Jeremy Hughes, John S Savill and 3 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 28 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

13 authors at 4 institutions in 1 country.

Agnes E CoutinhoCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
Tiina M J KipariCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
Zhenguang ZhangCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
Cristina L EstevesCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
Christopher D LucasCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
James S GilmourCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
Scott P WebsterCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
Brian R WalkerCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
Jeremy HughesCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
John S SavillCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
Jonathan R SecklCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
Adriano G RossiCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
Karen E ChapmanCentre for Cardiovascular Science (A.E.C., T.M.J.K., Z.Z., C.L.E., J.S.G., S.P.W., B.R.W., J.R.S., K.E.C.) and Medical Research Council Centre for Inflammation Research (A.E.C., C.D.L., J.S.G., J.H., J.S.S., A.G.R.), Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
University of Edinburgh · GBThe Queen's Medical Research Institute · GBMedical Research Council · GBCentre for Inflammation Research · GB

Funding

British Heart Foundation RG/11/4/28734Medical Research Council G0601481Medical Research Council G0800235Medical Research Council G0802069Medical Research Council MR/K013386/1Wellcome Trust
6 · The paper itself

Abstract

Endogenous glucocorticoid action within cells is enhanced by prereceptor metabolism by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which converts intrinsically inert cortisone and 11-dehydrocorticosterone into active cortisol and corticosterone, respectively. 11β-HSD1 is highly expressed in immune cells elicited to the mouse peritoneum during thioglycollate-induced peritonitis and is down-regulated as the inflammation resolves. During inflammation, 11β-HSD1-deficient mice show enhanced recruitment of inflammatory cells and delayed acquisition of macrophage phagocytic capacity. However, the key cells in which 11β-HSD1 exerts these effects remain unknown. Here we have identified neutrophils (CD11b(+),Ly6G(+),7/4(+) cells) as the thioglycollate-recruited cells that most highly express 11β-HSD1 and show dynamic regulation of 11β-HSD1 in these cells during an inflammatory response. Flow cytometry showed high expression of 11β-HSD1 in peritoneal neutrophils early during inflammation, declining at later states. In contrast, expression in blood neutrophils continued to increase during inflammation. Ablation of monocytes/macrophages by treatment of CD11b-diphtheria-toxin receptor transgenic mice with diphtheria toxin prior to thioglycollate injection had no significant effect on 11β-HSD1 activity in peritoneal cells, consistent with neutrophils being the predominant 11β-HSD1 expressing cell type at this time. Similar to genetic deficiency in 11β-HSD1, acute inhibition of 11β-HSD1 activity during thioglycollate-induced peritonitis augmented inflammatory cell recruitment to the peritoneum. These data suggest that neutrophil 11β-HSD1 increases during inflammation to contribute to the restraining effect of glucocorticoids upon neutrophil-mediated inflammation. In human neutrophils, lipopolysaccharide activation increased 11β-HSD1 expression, suggesting the antiinflammatory effects of 11β-HSD1 in neutrophils may be conserved in humans.

Indexed as

11-beta-Hydroxysteroid Dehydrogenase Type 1AnimalsHumansInflammationMacrophagesMaleMiceMice, TransgenicNeutrophils11-beta-Hydroxysteroid Dehydrogenase Type 1

Identifiers

PMID27145012
PMCPMC4929552
OpenAlexW2346142947

What OpenQuestion holds

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LicenceCC BY
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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.