Evidence map›Paper›PMID 20042590›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Critical protective role for MCP-1 in pneumonic Burkholderia mallei infection.

Andrew Goodyear, Abby Jones, Ryan Troyer, Helle Bielefeldt-Ohmann, Steven Dow

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Inhibition of macrophage infectivity potentiator inFrontiers in cellular and infection microbiology · 2024
    Article
  2. MCP-1: Function, regulation, and involvement in disease.International immunopharmacology · 2021
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Development of Burkholderia mallei and pseudomallei vaccines.Frontiers in cellular and infection microbiology · 2013
    Review
  12. Suppression of vaccine immunity by inflammatory monocytes.Journal of immunology (Baltimore, Md. : 1950) · 2012
    Article
  13. Article
  14. Article
  15. 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

5 authors at 1 institution in 1 country.

Andrew GoodyearDepartment of Microbiology, Immunology, and Pathology, Colorado State University, Ft. Collins, CO 80523, USA.
Abby Jones
Ryan Troyer
Helle Bielefeldt-Ohmann
Steven Dow
Colorado State University · US

Funding

Vascular stabilization as a broad theraprutic platform for biodefenseU54AI065357 · NIAID · COLORADO STATE UNIVERSITY-FORT COLLINS · PI SCHWEIZER, HERBERT P. · 2005 to 2013
$77.5M
NIAID NIH HHS U54 AI065357NIAID NIH HHS U54 AI065357-01
6 · The paper itself

Abstract

Burkholderia mallei is a gram-negative bacterial pathogen of domestic equidae and humans that can cause severe, rapidly life-threatening pneumonic infections. Little is known regarding the role of chemokines and early cellular immune responses in protective immunity to pulmonary infection with B. mallei. Although the role of MCP-1 in gram-positive bacterial infections has been previously investigated, the role of MCP-1 in immunity to acute pneumonia caused by gram-negative bacteria, such as B. mallei, has not been assessed. In a mouse model of pneumonic B. mallei infection, we found that both MCP-1(-/-) mice and CCR2(-/-) mice were extremely susceptible to pulmonary infection with B. mallei, compared with wild-type (WT) C57Bl/6 mice. Bacterial burden and organ lesions were significantly increased in CCR2(-/-) mice, compared with WT animals, following B. mallei challenge. Monocyte and dendritic cell recruitment into the lungs of CCR2(-/-) mice was significantly reduced in comparison with that in WT mice following B. mallei infection, whereas neutrophil recruitment was actually increased. Depletion of monocytes and macrophages prior to infection also greatly raised the susceptibility of WT mice to infection. Production of IL-12 and IFN-gamma in the lungs after B. mallei infection was significantly impaired in both MCP-1(-/-) and CCR2(-/-) mice, whereas treatment of CCR2(-/-) mice with rIFN-gamma restored protection against lethal challenge with B. mallei. Thus, we conclude that MCP-1 plays a key role in regulating cellular immunity and IFN-gamma production following pneumonic infection with B. mallei and therefore may also figure importantly in other gram-negative pneumonias.

Indexed as

AnimalsBurkholderia InfectionsBurkholderia malleiCell MovementChemokine CCL2Genetic Predisposition to DiseaseImmunity, CellularInterferon-gammaMacrophagesMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMonocytesNeutrophil InfiltrationPneumonia, BacterialCcl2 protein, mouseCcr2 protein, mouseChemokine CCL2Interferon-gammaReceptors, CCR2

Identifiers

PMID20042590
PMCPMC2878842
OpenAlexW2100354143

What OpenQuestion holds

Textmetadata
LicenceTDM
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.