Evidence map›Paper›PMID 22246861›Full record

ArticleAmerican journal of respiratory cell and molecular biology2012

Resistin-like molecule-α regulates IL-13-induced chemokine production but not allergen-induced airway responses.

Ariel Munitz, Eric T Cole, Danielle Karo-Atar, Fred D Finkelman, Marc E Rothenberg

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 39 citations in OpenAlex.

  1. Mechanisms and therapeutic strategies of asthma: from bench to bedside.Signal transduction and targeted therapy · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Resistin family proteins in pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Resistin-Like Molecule α in Allergen-Induced Pulmonary Vascular Remodeling.American journal of respiratory cell and molecular biology · 2015
    Article
  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 3 institutions in 2 countries.

Ariel MunitzDivision of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Ave., Cincinnati, OH 45229, USA.
Eric T Cole
Danielle Karo-Atar
Fred D Finkelman
Marc E Rothenberg
Cincinnati Children's Hospital Medical Center · USTel Aviv University · ILUniversity of Cincinnati · US

Funding

REGULATION OF GASTROINTESTINAL EOSINOPHILSR01AI045898 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 1999 to 2024
$4.5M
Regulation of Gastrointestinal EosinophilsR37AI045898 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 2010 to 2019
$3.6M
IL-13 and Eosinophilic EsophagitisR01DK076893 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 2007 to 2011
$3.1M
IL-13 Associated Eosinophil Lung ResponsesR01AI083450 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 2009 to 2013
$1.9M
Direct IL-4 and IL-13 effects on pulmonary smooth muscle in allergic airway diseaR01HL097360 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI FINKELMAN, FRED DOUGLASS · 2009 to 2010
$951k
NHLBI NIH HHS R01 HL097360NIAID NIH HHS R01 AI045898NIAID NIH HHS R01 AI083450NIAID NIH HHS R37 AI045898NIDDK NIH HHS R01 DK076893
6 · The paper itself

Abstract

Resistin-like molecule α (Relm-α) is one of the most up-regulated gene products in allergen- and parasite-associated Th2 responses. Localized to alternatively activated macrophages, Relm-α was shown to exert an anti-inflammatory effect in parasite-induced Th2 responses, but its role in experimental asthma remains unexplored. Here, we analyzed the cellular source, the IL-4 receptors required to stimulate Relm-α production, and the role of Relm-α after experimental asthma induction by IL-4, IL-13, or multiple experimental regimes, including ovalbumin and Aspergillus fumigatus immunization. We demonstrate that Relm-α was secreted into the airway lumen, dependent on both the IL-13 receptor-α1 chain and likely the Type I IL-4 receptor, and differentially localized to epithelial cells and myeloid cells, depending on the specific cytokine or aeroallergen trigger. Studies performed with Retnla gene-targeted mice demonstrate that Relm-α was largely redundant in terms of inducing the infiltration of Th2 cytokines, mucus, and inflammatory cells into the lung. These results mirror the dispensable role that other alternatively activated macrophage products (such as arginase 1) have in allergen-induced experimental asthma and contrast with their role in the setting of parasitic infections. Taken together, our findings demonstrate the distinct utilization of IL-4/IL-13 receptors for the induction of Relm-α in the lungs. The differential regulation of Relm-α expression is likely determined by the relative expression levels of IL-4, IL-13, and their corresponding receptors, which are differentially expressed by divergent cells (i.e., epithelial cells and macrophages.) Finally, we identify a largely redundant functional role for Relm-α in acute experimental models of allergen-associated Th2 immune responses.

Indexed as

AllergensAnimalsAsthmaBronchoalveolar Lavage FluidChemokinesEnzyme-Linked Immunosorbent AssayIntercellular Signaling Peptides and ProteinsInterleukin-13MiceReal-Time Polymerase Chain ReactionAllergensChemokinesIntercellular Signaling Peptides and ProteinsInterleukin-13Retnla protein, mouse

Identifiers

PMID22246861
PMCPMC3359904
OpenAlexW2107088747

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.