Evidence map›Paper›PMID 22564028›Full record

ArticleImmunology2012

Extracellular ATP-stimulated macrophages produce macrophage inflammatory protein-2 which is important for neutrophil migration.

Hiroki Kawamura, Toshihiko Kawamura, Yasuhiro Kanda, Takahiro Kobayashi, Toru Abo

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 58 citations in OpenAlex.

  1. Trial
  2. Article
  3. Cleavage-Resistant CYLD Protects Against Autoimmune Hepatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Genetic Deletion of the Purinergic ReceptorACS pharmacology & translational science · 2025
    Article
  8. Article
  9. Article
  10. Physiologic roles of P2 receptors in leukocytes.Journal of leukocyte biology · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Extracellular release of ATP promotes systemic inflammation during acute pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2019
    Article
  18. ATP redirects cytokine trafficking and promotes novel membrane TNF signalingFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  19. Review
  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

5 authors at 1 institution in 1 country.

Hiroki KawamuraDivision of Immunology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. h-kawa@med.niigata-u.ac.jp
Toshihiko Kawamura
Yasuhiro Kanda
Takahiro Kobayashi
Toru Abo
Niigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages are the major source of the chemokines macrophage inflammatory protein-2 (MIP-2) and keratinocyte-derived chemokine (KC), which play a major role in neutrophil migration to sites of inflammation. Although extracellular ATP from inflammatory tissues induces several immune responses in macrophages, it is unclear whether ATP-stimulated macrophages affect neutrophil migration. Therefore, the aim of the present study was to investigate the role of ATP-induced MIP-2 production by macrophages. When ATP was injected intraperitoneally into mice, the number of neutrophils within the peritoneal cavity markedly increased, along with the levels of MIP-2 and KC in the peritoneal lavage fluid. Consistent with this, ATP induced MIP-2 production, but not that of KC, by peritoneal exudate macrophages (PEMs) in vitro. This occurred via interactions with the P2X(7) receptor and P2Y(2) receptor. Furthermore, treatment of PEMs with ATP led to the production of reactive oxygen species. The ATP-induced MIP-2 production was inhibited by treatment with the antioxidant N-acetyl-l-cysteine. Also, MIP-2 production was inhibited by pre-incubating PEMs with inhibitors of extracellular signal-regulated kinase 1/2 or p38 mitogen-activated protein kinase. The MIP-2 neutralization reduced the increase in neutrophil numbers observed in ATP-treated mice. Taken together, these results suggest that increased production of reactive oxygen species by ATP-stimulated macrophages activates the signalling pathways that promote MIP-2 production which, in turn, induces neutrophil migration.

Indexed as

Chemotaxis, LeukocyteAcetylcysteineAdenosine TriphosphateAnimalsCell MovementCells, CulturedChemokine CXCL2ChemokinesExtracellular Signal-Regulated MAP KinasesMacrophages, PeritonealMiceMice, Inbred C57BLMice, TransgenicNeutrophilsp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesAcetylcysteineAdenosine TriphosphateChemokine CXCL2ChemokinesExtracellular Signal-Regulated MAP Kinaseskeratinocyte-derived chemokinesp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesReceptors, Purinergic P2X7Receptors, Purinergic P2Y2

Identifiers

PMID22564028
PMCPMC3401983
OpenAlexW1579600243

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.