Evidence map›Paper›PMID 29847178›Full record

ArticleDrug delivery2018

Biomimetic carbon monoxide delivery based on hemoglobin vesicles ameliorates acute pancreatitis in mice via the regulation of macrophage and neutrophil activity.

Kazuaki Taguchi, Saori Nagao, Hitoshi Maeda, Hiroki Yanagisawa, Hiromi Sakai, Keishi Yamasaki, Tomohiko Wakayama, Hiroshi Watanabe, Masaki Otagiri, Toru Maruyama

Open access · goldAbstract read
In one paragraph

Article in Drug delivery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. The Triple Crown: NO, CO, and HPharmacology & therapeutics · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
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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

10 authors at 3 institutions in 1 country.

Kazuaki Taguchia Faculty of Pharmaceutical Sciences , Sojo University , Kumamoto , Japan.
Saori Nagaob Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences , Kumamoto University , Kumamoto , Japan.
Hitoshi Maedab Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences , Kumamoto University , Kumamoto , Japan.
Hiroki Yanagisawab Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences , Kumamoto University , Kumamoto , Japan.
Hiromi Sakaic Department of Chemistry , Nara Medical University , Kashihara , Japan.
Keishi Yamasakia Faculty of Pharmaceutical Sciences , Sojo University , Kumamoto , Japan.
Tomohiko Wakayamae Department of Histology, Graduate School of Medical Sciences , Kumamoto University , Kumamoto , Japan.
Hiroshi Watanabeb Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences , Kumamoto University , Kumamoto , Japan.
Masaki Otagiria Faculty of Pharmaceutical Sciences , Sojo University , Kumamoto , Japan.
Toru Maruyamab Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences , Kumamoto University , Kumamoto , Japan.
Kumamoto University · JPSojo University · JPNara Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages play a central role in various inflammatory disorders and are broadly divided into two subpopulations, M1 and M2 macrophage. In the healing process in acute inflammatory disorders, shifting the production of M1 macrophages to M2 macrophages is desirable, because M1 macrophages secrete pro-inflammatory cytokines, whilst the M2 variety secrete anti-inflammatory cytokines. Previous findings indicate that when macrophages are treated with carbon monoxide (CO), the secretion of anti-inflammatory cytokine is increased and the expression of pro-inflammatory cytokines is inhibited, indicating that CO may have a potential to modulate the production of macrophages toward the M2-like phenotype. In this study, we examined the issue of whether CO targeting macrophages using a nanotechnology-based CO donor, namely CO-bound hemoglobin vesicles (CO-HbV), modulates their polarization and show therapeutic effects against inflammatory disorders. The results showed that the CO-HbV treatment polarized a macrophage cell line toward an M2-like phenotype. Furthermore, in an in vivo study using acute pancreatitis model mice as a model of an inflammatory disease, a CO-HbV treatment also tended to polarize macrophages toward an M2-like phenotype and inhibited neutrophil infiltration in the pancreas, resulting in a significant inflammation. In addition to the suppression of acute pancreatitis, CO-HbV diminished a subsequent pancreatitis-associated acute lung injury. This could be due to the inhibition of the systemic inflammation, neutrophil infiltration in the lungs and the production of HMGB-1. These findings suggest that CO-HbV exerts superior anti-inflammatory effects against inflammatory disorders via the regulation of macrophage and neutrophil activity.

Indexed as

AnimalsAnti-Inflammatory AgentsBiomimeticsCarbon MonoxideCell LineCytokinesDisease Models, AnimalHemoglobinsInflammationMacrophagesMaleMiceMice, Inbred C57BLNeutrophilsPancreasPancreatitisAnti-Inflammatory AgentsCarbon MonoxideCytokinesHemoglobinsacute pancreatitiscarbon monoxideliposomeMacrophagepolarization

Identifiers

PMID29847178
PMCPMC6058524
OpenAlexW2805624241

What OpenQuestion holds

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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.