Evidence map›Paper›PMID 25486994›Full record

ArticleInfection and immunity2015

Impact of resolvin E1 on murine neutrophil phagocytosis in type 2 diabetes.

Bruno S Herrera, Hatice Hasturk, Alpdogan Kantarci, Marcelo O Freire, Olivia Nguyen, Shevali Kansal, Thomas E Van Dyke

Abstract 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 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
–field-weighted citation impact
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

56 citing papers in PubMed.

  1. Trial
  2. Plasma Resolvin D2 to Leukotriene BBioMed research international · 2021
    Trial
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Resolving neutrophils due to TRAM deletion renders protection against experimental sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  10. Article
  11. Article
  12. Roles of Resolvins in Chronic Inflammatory Response.International journal of molecular sciences · 2022
    Review
  13. Article
  14. Modeling human heterogeneity of obesity with diversity outbred mice reveals a fat mass-dependent therapeutic window for resolvin E1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  15. Review
  16. Review
  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

7 authors.

Bruno S HerreraDepartment of Applied Oral Sciences, Forsyth Institute, Cambridge, Massachusetts, USA.
Hatice HasturkDepartment of Applied Oral Sciences, Forsyth Institute, Cambridge, Massachusetts, USA.
Alpdogan KantarciDepartment of Applied Oral Sciences, Forsyth Institute, Cambridge, Massachusetts, USA.
Marcelo O FreireDepartment of Applied Oral Sciences, Forsyth Institute, Cambridge, Massachusetts, USA.
Olivia NguyenDepartment of Applied Oral Sciences, Forsyth Institute, Cambridge, Massachusetts, USA.
Shevali KansalDepartment of Applied Oral Sciences, Forsyth Institute, Cambridge, Massachusetts, USA.
Thomas E Van DykeDepartment of Applied Oral Sciences, Forsyth Institute, Cambridge, Massachusetts, USA tvandyke@forsyth.org.

Funding

Neutrophils and Periodontitis in DiabetesR01DE015566 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI VAN DYKE, THOMAS ELLIOTT · 2005 to 2014
$4.2M
Regulation of ChemR23 in Resolution of InflammationR00DE023584 · NIDCR · J. CRAIG VENTER INSTITUTE, INC. · PI FREIRE, MARCELO · 2015 to 2019
$1.2M
Treatment of Periodontitis and Inflammatory Changes in DiabetesK23DE018917 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HASTURK, HATICE · 2008 to 2012
$647k
Regulation of ChemR23 in Resolution of InflammationK99DE023584 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI FREIRE, MARCELO · 2013 to 2014
$207k
NIDCR NIH HHS DE015566NIDCR NIH HHS DE018917NIDCR NIH HHS DE023584NIDCR NIH HHS K23 DE018917NIDCR NIH HHS K99 DE023584NIDCR NIH HHS R00 DE023584NIDCR NIH HHS R01 DE015566
6 · The paper itself

Abstract

Diabetic complications involve inflammation-mediated microvascular and macrovascular damage, disruption of lipid metabolism, glycosylation of proteins, and abnormalities of neutrophil-mediated events. Resolution of inflamed tissues to health and homeostasis is an active process mediated by endogenous lipid agonists, including lipoxins and resolvins. This proresolution system appears to be compromised in type 2 diabetes (T2D). The goal of this study was to investigate unresolved inflammation in T2D. Wild-type (WT) and genetically engineered mice, including T2D mice (db/db), transgenic mice overexpressing the human resolvin E1 (RvE1) receptor (ERV1), and a newly bred strain of db/ERV1 mice, were used to determine the impact of RvE1 on the phagocytosis of Porphyromonas gingivalis in T2D. Neutrophils were isolated and incubated with fluorescein isothiocyanate-labeled P. gingivalis, and phagocytosis was measured in a fluorochrome-based assay by flow cytometry. Mitogen-activated protein kinase (MAPK) (p42 and p44) and Akt (Thr308 and Ser473) phosphorylation was analyzed by Western blotting. The mouse dorsal air pouch model was used to evaluate the in vivo impact of RvE1. Results revealed that RvE1 increased the neutrophil phagocytosis of P. gingivalis in WT animals but had no impact in db/db animals. In ERV1-transgenic and ERV1-transgenic diabetic mice, phagocytosis was significantly increased. RvE1 decreased Akt and MAPK phosphorylation in the transgenic animals. In vivo dorsal air pouch studies revealed that RvE1 decreases neutrophil influx into the pouch and increases neutrophil phagocytosis of P. gingivalis in the transgenic animals; cutaneous fat deposition was reduced, as was macrophage infiltration. The results suggest that RvE1 rescues impaired neutrophil phagocytosis in obese T2D mice overexpressing ERV1.

Indexed as

AnimalsBacteroidaceae InfectionsBlood GlucoseDiabetes ComplicationsDiabetes Mellitus, Type 2Eicosapentaenoic AcidFlow CytometryGlycosylationInflammationLipid MetabolismMaleMiceMice, ObeseMice, TransgenicMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 35S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acidBlood GlucoseEicosapentaenoic AcidMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3

Identifiers

PMID25486994
PMCPMC4294250

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Registered trials

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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.