Evidence map›Paper›PMID 15377395›Full record

ArticleRespiratory research2004

Aspergillus antigen induces robust Th2 cytokine production, inflammation, airway hyperreactivity and fibrosis in the absence of MCP-1 or CCR2.

Laura L Koth, Madeleine W Rodriguez, Xin Liu Bernstein, Salina Chan, Xiaozhu Huang, Israel F Charo, Barrett J Rollins, David J Erle

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Inactivation of the gene encoding procalcitonin prevents antibody-mediated arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  2. Article
  3. Article
  4. Type 2 immunity in tissue repair and fibrosis.Nature reviews. Immunology · 2018
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Neonatal hyperoxia alters the host response to influenza A virus infection in adult mice through multiple pathways.American journal of physiology. Lung cellular and molecular physiology · 2013
    Article
  11. Article
  12. Article
  13. A protective role for periostin and TGF-β in IgE-mediated allergy and airway hyperresponsiveness.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2012
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

8 authors at 3 institutions in 1 country.

Laura L KothLung Biology Center, Department of Medicine, University of California, San Francisco, California, USA. lkoth@itsa.ucsf.edu <lkoth@itsa.ucsf.edu>
Madeleine W Rodriguez
Xin Liu Bernstein
Salina Chan
Xiaozhu Huang
Israel F Charo
Barrett J Rollins
David J Erle
University of California, San Francisco · USGladstone Institutes · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAsthma is characterized by type 2 T-helper cell (Th2) inflammation, goblet cell hyperplasia, airway hyperreactivity, and airway fibrosis. Monocyte chemoattractant protein-1 (MCP-1 or CCL2) and its receptor, CCR2, have been shown to play important roles in the development of Th2 inflammation. CCR2-deficient mice have been found to have altered inflammatory and physiologic responses in some models of experimental allergic asthma, but the role of CCR2 in contributing to inflammation and airway hyperreactivity appears to vary considerably between models. Furthermore, MCP-1-deficient mice have not previously been studied in models of experimental allergic asthma.

methodsTo test whether MCP-1 and CCR2 are each required for the development of experimental allergic asthma, we applied an Aspergillus antigen-induced model of Th2 cytokine-driven allergic asthma associated with airway fibrosis to mice deficient in either MCP-1 or CCR2. Previous studies with live Aspergillus conidia instilled into the lung revealed that MCP-1 and CCR2 play a role in anti-fungal responses; in contrast, we used a non-viable Aspergillus antigen preparation known to induce a robust eosinophilic inflammatory response.

resultsWe found that wild-type C57BL/6 mice developed eosinophilic airway inflammation, goblet cell hyperplasia, airway hyperreactivity, elevations in serum IgE, and airway fibrosis in response to airway challenge with Aspergillus antigen. Surprisingly, mice deficient in either MCP-1 or CCR2 had responses to Aspergillus antigen similar to those seen in wild-type mice, including production of Th2 cytokines.

conclusionWe conclude that robust Th2-mediated lung pathology can occur even in the complete absence of MCP-1 or CCR2.

Indexed as

AnimalsAntigens, FungalAspergillosis, Allergic BronchopulmonaryAspergillus fumigatusBronchial HyperreactivityChemokine CCL2CytokinesEosinophiliaFibrosisMiceMice, KnockoutReceptors, CCR2Receptors, ChemokineTh2 CellsAntigens, FungalCcl2 protein, mouseCcr2 protein, mouseChemokine CCL2CytokinesReceptors, CCR2Receptors, Chemokine

Identifiers

PMID15377395
PMCPMC520828
OpenAlexW2140829143

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.