Evidence map›Paper›PMID 28675904›Full record

ArticleJournal of innate immunity2017

In vivo Lipopolysaccharide Tolerance Recruits CD11b+ Macrophages to the Liver with Enhanced Bactericidal Activity and Low Tumor Necrosis Factor-Releasing Capability, Resulting in Drastic Resistance to Lethal Septicemia.

Manabu Kinoshita, Hiromi Miyazaki, Hiroyuki Nakashima, Masahiro Nakashima, Makoto Nishikawa, Takuya Ishikiriyama, Shoichiro Kato, Keiichi Iwaya, Sadayuki Hiroi, Nariyoshi Shinomiya and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of innate immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Role of T cells in liver metastasis.Cell death & disease · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Tackling the Pros and Cons of Inflammation.Journal of innate immunity · 2019
    Article
  14. The Extracellular Matrix: Reloaded Revolutions.Journal of innate immunity · 2019
    Article
  15. Review
  16. With Complement.Journal of innate immunity · 2018
    Article
  17. 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

11 authors at 5 institutions in 2 countries.

Manabu KinoshitaDepartment of Immunology and Microbiology, National Defense Medical College, Tokorozawa, Japan.
Hiromi Miyazaki
Hiroyuki Nakashima
Masahiro Nakashima
Makoto Nishikawa
Takuya Ishikiriyama
Shoichiro Kato
Keiichi Iwaya
Sadayuki Hiroi
Nariyoshi Shinomiya
Shuhji Seki
Bipar · FRNational Defense Medical College · JPNational Defense Medical College Hospital · JPNitobe Bunka College · JPSasaki Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesIn vivo lipopolysaccharide (LPS) tolerance on bacterial infection was investigated, focusing on liver macrophages.

methodsLPS tolerance was induced by intraperitoneal injections with 5 μg/kg of LPS for 3 consecutive days, and then mice were intravenously infected with Escherichia coli.

resultsAll LPS-primed mice survived lethal bacterial infection. Drastic enhancement of bactericidal activity of liver macrophages strongly contributed to bacterial clearance. Although LPS-primed mice produced substantial amounts of tumor necrosis factor (TNF) inside the liver, TNF efflux into the systemic circulation was markedly suppressed. These mice showed a dramatic increase in CD11b+ monocyte- derived macrophages in the liver. The CD11b+ macrophages that increased in LPS-primed mice were those with strong phagocytic/bactericidal activity and an upregulated expression of Fcγ receptor I, but the subfraction with a potent TNF-producing capacity and poor phagocytic activity diminished. The adoptive transfer of CD11b+ macrophages from LPS-primed mice to control mice increased survival after bacterial infection and reduced the elevation of plasma TNF. LPS priming did not affect the CD68+ resident Kupffer cells, and CD68+ Kupffer cell-depleted mice still exhibited LPS tolerance with strong resistance to bacteremia.

conclusionsLPS tolerance recruits CD11b+ macrophages to the liver with enhanced bactericidal activity, which plays a central role in resistance to lethal bacteremia.

Indexed as

AnimalsBacteriolysisCD11b AntigenCell MovementCells, CulturedEscherichia coliEscherichia coli InfectionsImmune ToleranceImmunityInjections, IntraperitonealLipopolysaccharidesLiverMacrophagesMaleMiceMice, Inbred C57BLCD11b AntigenFcgr1 protein, mouseLipopolysaccharidesReceptors, IgGTumor Necrosis Factor-alphaBacterial septicemiaCD11b+Escherichia coli infectionLipopolysaccharide toleranceMonocyte-derived macrophagesTumor necrosis factor

Identifiers

PMID28675904
PMCPMC6738816
OpenAlexW2727765604

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.