Evidence map›Paper›PMID 21653234›Full record

ArticleJournal of leukocyte biology2011

17(R)-Resolvin D1 differentially regulates TLR4-mediated responses of primary human macrophages to purified LPS and live E. coli.

Christine D Palmer, Christy J Mancuso, Jerrold P Weiss, Charles N Serhan, Eva C Guinan, Ofer Levy

Abstract read
In one paragraph

Article in Journal of leukocyte biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
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

31 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Resolvin D2 decreases TLR4 expression to mediate resolution in human monocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  17. Article
  18. ResolvinD1 reduces apoptosis and inflammation in primary human alveolar epithelial type 2 cells.Laboratory investigation; a journal of technical methods and pathology · 2016
    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

6 authors at 4 institutions in 1 country.

Christine D PalmerChildren's Hospital Boston, Boston, MA 02115, USA.
Christy J Mancuso
Jerrold P Weiss
Charles N Serhan
Eva C Guinan
Ofer Levy
Harvard University · USBoston Children's Hospital · USDana-Farber Cancer Institute · USUniversity of Iowa · US

Funding

Resolution Mechanisms in Acute Inflammation: Resolution PharmacologyP01GM095467 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI PETASIS, NICOS A · 2011 to 2020
$14.8M
BLOOD CELL LIPOXYGENASE PRODUCTS: FORMATION AND ACTIONR01GM038765 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 1992 to 2020
$4.9M
Adenosine Shapes Neonatal Toll-like Receptor FunctionR01AI067353 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI LEVY, OFER · 2006 to 2010
$2.1M
rBPI21 & Endotoxin-directed Innate Immunity in Stem Cell TransplantationR21HL089659 · NHLBI · DANA-FARBER CANCER INST · PI GUINAN, EVA C · 2008 to 2009
$489k
NHLBI NIH HHS R21 HL089659NIAID NIH HHS 3R01AI067353-05S1NIAID NIH HHS R01 AI067353NIGMS NIH HHS P01 GM095467NIGMS NIH HHS P01GM095467NIGMS NIH HHS R01 GM038765NIGMS NIH HHS R01GM038765
6 · The paper itself

Abstract

Detection and clearance of bacterial infection require balanced effector and resolution signals to avoid chronic inflammation. Detection of GNB LPS by TLR4 on m induces inflammatory responses, contributing to chronic inflammation and tissue injury. LXs and Rvs are endogenous lipid mediators that enhance resolution of inflammation, and their actions on primary human m responses toward GNB are largely uncharacterized. Here, we report that LXA(4), LXB(4), and RvD1, tested at 0.1-1 μM, inhibited LPS-induced TNF production from primary human m, with ATL and 17(R)-RvD1, demonstrating potent inhibition at 0.1 μM. In addition, 17(R)-RvD1 inhibited LPS-induced primary human m production of IL-7, IL-12p70, GM-CSF, IL-8, CCL2, and MIP-1α without reducing that of IL-6 or IL-10. Remarkably, when stimulated with live Escherichia coli, m treated with 17(R)-RvD1 demonstrated increased TNF production and enhanced internalization and killing of the bacteria. 17(R)-RvD1-enhanced TNF, internalization, and killing were not evident for an lpxM mutant of E. coli expressing hypoacylated LPS with reduced inflammatory activity. Furthermore, 17(R)-RvD1-enhanced, E. coli-induced TNF production was evident in WT but not TLR4-deficient murine m. Thus, Rvs differentially modulate primary human m responses to E. coli in an LPS- and TLR4-dependent manner, such that this Rv could promote resolution of GNB/LPS-driven inflammation by reducing m proinflammatory responses to isolated LPS and increasing m responses important for clearance of infection.

Indexed as

AnimalsBlotting, WesternCell Adhesion MoleculesCell DifferentiationCell ProliferationCytokinesDocosahexaenoic AcidsEnzyme-Linked Immunosorbent AssayEscherichia coliEscherichia coli InfectionsHumansInflammation MediatorsLipopolysaccharidesMacrophagesMiceMutationCell Adhesion MoleculesCytokinesDocosahexaenoic AcidsInflammation MediatorsLipopolysaccharidesLPXN protein, humanPhosphoproteinsresolvin D1RNA, MessengerToll-Like Receptor 4

Identifiers

PMID21653234
PMCPMC3157902
OpenAlexW1986273261

What OpenQuestion holds

Textmetadata
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.