Evidence map›Paper›PMID 19203252›Full record

ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2009

CCL26-targeted siRNA treatment of alveolar type II cells decreases expression of CCR3-binding chemokines and reduces eosinophil migration: implications in asthma therapy.

Younes J Errahali, Equar Taka, Barack O Abonyo, Ann S Heiman

Open access · greenAbstract read
In one paragraph

Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Protein-Protein interactive networks identified in bronchoalveolar lavage of severe compared to nonsevere asthma.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2024
    Article
  3. Review
  4. Article
  5. Article
  6. Inhibition by new glucocorticoid antedrugs [16α, 17α-d] isoxazoline and [16α, 17α-d]-3'-hydroxy-iminoformyl isoxazoline derivatives of chemotaxis and CCL26, CCL11, IL-8, and RANTES secretion.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2013
    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

4 authors at 1 institution in 1 country.

Younes J ErrahaliCollege of Pharmacy and Pharmaceutical Sciences, Florida A&M University, Tallahassee, Florida 32307, USA.
Equar Taka
Barack O Abonyo
Ann S Heiman
Florida Agricultural and Mechanical University · US

Funding

THE PREVENTION OF B(A)P INDUCED CELL TRANSFORMATION BY ORGANOSULFUR COMPOUNDSG12RR003020 · NCRR · FLORIDA AGRICULTURAL AND MECHANICAL UNIV · PI DARLING-REED, SELINA FAITH · 1985 to 2011
$29.7M
Targeted Nanocarrier Combination Based Therapy for Lung CancerP20MD006738 · NIMHD · FLORIDA AGRICULTURAL AND MECHANICAL UNIV · PI RAHMAN, SALEH MD. MAHMUDUR · 2012 to 2016
$5.6M
IDENTIFICATION OF EOTAXIN-3 REGULATED GENES AND PROTEINS IN ALVEOLAR TYPE II CELLR15HL093710 · NHLBI · FLORIDA AGRICULTURAL AND MECHANICAL UNIV · PI ABONYO, BARACK OTIENO · 2009 to 2009
$213k
UNSATURATED KETODEOXY HEXOSYL AZAURACILS-ANTICANCER AGENTSS06RR008111 · NCRR · FLORIDA AGRICULTURAL AND MECHANICAL UNIV · PI REDDA, KEN · 1985 to 1989
–
NCRR NIH HHS G12 RR003020NCRR NIH HHS RR03020NCRR NIH HHS RR08111NHLBI NIH HHS R15 HL093710NIMHD NIH HHS P20 MD006738
6 · The paper itself

Abstract

The underlying inflammation present in chronic airway diseases is orchestrated by increased expression of CC chemokines that selectively recruit leukocyte populations into the pulmonary system. Human CCL26 signals through CC chemokine receptor 3 (CCR3), is dramatically upregulated in challenged asthmatics, and stimulates recruitment of eosinophils (EOSs) and other leukocytes. CCL26 participates in regulation of its receptor CCR3 and modulates expression of a variety of chemokines in alveolar type II cells. Utilizing the A549 alveolar type II epithelial cell culture model, we carried out studies to test the hypothesis that CCL26-siRNA treatment of these cells would ameliorate Th2-driven release of the eotaxins and other CCR3 ligands that would, in turn, decrease recruitment and activation of EOSs. Results demonstrate that CCL26-siRNA treatments decreased interleukin-4-induced CCL26 and CCL24 expression by >70%. CCL26-directed small-interfering RNA (siRNA) treatments significantly decreased release of CCL5 (RANTES), CCL15 (MIP-1δ), CCL8 (MCP-2), and CCL13 (MCP-4). In bioactivity assays it was shown that EOS migration and activation were reduced up to 80% and 90%, respectively, when exposed to supernatants of CCL26-siRNA-treated cells. These results provide evidence that CCL26 may be an appropriate target for development of new therapeutic agents designed to alleviate the underlying inflammation associated with chronic diseases of the airways.

Indexed as

Cell MovementAsthmaCells, CulturedChemokine CCL26Chemokines, CCEosinophilsEpithelial CellsHumansPulmonary AlveoliReceptors, CCR3RNA, MessengerRNA, Small InterferingCCL26 protein, humanChemokine CCL26Chemokines, CCReceptors, CCR3RNA, MessengerRNA, Small Interfering

Identifiers

PMID19203252
PMCPMC2941665
OpenAlexW2064610968

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.