Coordinated post-transcriptional regulation of the chemokine system: Messages from CCL2

Ronaldo P. Panganiban, Becky Marie Vonakis, Faoud T. Ishmael, Cristiana Stellato

Research output: Contribution to journalArticle

Abstract

The molecular cross-talk between epithelium and immune cells in the airway mucosa is a key regulator of homeostatic immune surveillance and is crucially involved in the development of chronic lung inflammatory diseases. The patterns of gene expression that follow the sensitization process occurring in allergic asthma and chronic rhinosinusitis and those present in the neutrophilic response of other chronic inflammatory lung diseases such as chronic obstructive pulmonary disease (COPD) are tightly regulated in their specificity. Studies exploring the global transcript profiles associated with determinants of post-transcriptional gene regulation (PTR) such as RNA-binding proteins (RBP) and microRNAs identified several of these factors as being crucially involved in controlling the expression of chemokines upon airway epithelial cell stimulation with cytokines prototypic of Th1-or Th2-driven responses. These studies also uncovered the participation of these pathways to glucocorticoids' inhibitory effect on the epithelial chemokine network. Unmasking the molecular mechanisms of chemokine PTR may likely uncover novel therapeutic strategies for the blockade of proinflammatory pathways that are pathogenetic for asthma, COPD, and other lung inflammatory diseases.

Original languageEnglish (US)
Pages (from-to)255-266
Number of pages12
JournalJournal of Interferon and Cytokine Research
Volume34
Issue number4
DOIs
StatePublished - Apr 1 2014

Fingerprint

Chemokines
Lung Diseases
Chronic Obstructive Pulmonary Disease
Asthma
RNA-Binding Proteins
MicroRNAs
Glucocorticoids
Genes
Mucous Membrane
Epithelium
Epithelial Cells
Cytokines
Gene Expression
Therapeutics

ASJC Scopus subject areas

  • Immunology
  • Virology
  • Cell Biology

Cite this

Coordinated post-transcriptional regulation of the chemokine system : Messages from CCL2. / Panganiban, Ronaldo P.; Vonakis, Becky Marie; Ishmael, Faoud T.; Stellato, Cristiana.

In: Journal of Interferon and Cytokine Research, Vol. 34, No. 4, 01.04.2014, p. 255-266.

Research output: Contribution to journalArticle

Panganiban, Ronaldo P. ; Vonakis, Becky Marie ; Ishmael, Faoud T. ; Stellato, Cristiana. / Coordinated post-transcriptional regulation of the chemokine system : Messages from CCL2. In: Journal of Interferon and Cytokine Research. 2014 ; Vol. 34, No. 4. pp. 255-266.
@article{896d8a36f8894d7fa7057eee29f5c7e3,
title = "Coordinated post-transcriptional regulation of the chemokine system: Messages from CCL2",
abstract = "The molecular cross-talk between epithelium and immune cells in the airway mucosa is a key regulator of homeostatic immune surveillance and is crucially involved in the development of chronic lung inflammatory diseases. The patterns of gene expression that follow the sensitization process occurring in allergic asthma and chronic rhinosinusitis and those present in the neutrophilic response of other chronic inflammatory lung diseases such as chronic obstructive pulmonary disease (COPD) are tightly regulated in their specificity. Studies exploring the global transcript profiles associated with determinants of post-transcriptional gene regulation (PTR) such as RNA-binding proteins (RBP) and microRNAs identified several of these factors as being crucially involved in controlling the expression of chemokines upon airway epithelial cell stimulation with cytokines prototypic of Th1-or Th2-driven responses. These studies also uncovered the participation of these pathways to glucocorticoids' inhibitory effect on the epithelial chemokine network. Unmasking the molecular mechanisms of chemokine PTR may likely uncover novel therapeutic strategies for the blockade of proinflammatory pathways that are pathogenetic for asthma, COPD, and other lung inflammatory diseases.",
author = "Panganiban, {Ronaldo P.} and Vonakis, {Becky Marie} and Ishmael, {Faoud T.} and Cristiana Stellato",
year = "2014",
month = "4",
day = "1",
doi = "10.1089/jir.2013.0149",
language = "English (US)",
volume = "34",
pages = "255--266",
journal = "Journal of Interferon and Cytokine Research",
issn = "1079-9907",
publisher = "Mary Ann Liebert Inc.",
number = "4",

}

TY - JOUR

T1 - Coordinated post-transcriptional regulation of the chemokine system

T2 - Messages from CCL2

AU - Panganiban, Ronaldo P.

AU - Vonakis, Becky Marie

AU - Ishmael, Faoud T.

AU - Stellato, Cristiana

PY - 2014/4/1

Y1 - 2014/4/1

N2 - The molecular cross-talk between epithelium and immune cells in the airway mucosa is a key regulator of homeostatic immune surveillance and is crucially involved in the development of chronic lung inflammatory diseases. The patterns of gene expression that follow the sensitization process occurring in allergic asthma and chronic rhinosinusitis and those present in the neutrophilic response of other chronic inflammatory lung diseases such as chronic obstructive pulmonary disease (COPD) are tightly regulated in their specificity. Studies exploring the global transcript profiles associated with determinants of post-transcriptional gene regulation (PTR) such as RNA-binding proteins (RBP) and microRNAs identified several of these factors as being crucially involved in controlling the expression of chemokines upon airway epithelial cell stimulation with cytokines prototypic of Th1-or Th2-driven responses. These studies also uncovered the participation of these pathways to glucocorticoids' inhibitory effect on the epithelial chemokine network. Unmasking the molecular mechanisms of chemokine PTR may likely uncover novel therapeutic strategies for the blockade of proinflammatory pathways that are pathogenetic for asthma, COPD, and other lung inflammatory diseases.

AB - The molecular cross-talk between epithelium and immune cells in the airway mucosa is a key regulator of homeostatic immune surveillance and is crucially involved in the development of chronic lung inflammatory diseases. The patterns of gene expression that follow the sensitization process occurring in allergic asthma and chronic rhinosinusitis and those present in the neutrophilic response of other chronic inflammatory lung diseases such as chronic obstructive pulmonary disease (COPD) are tightly regulated in their specificity. Studies exploring the global transcript profiles associated with determinants of post-transcriptional gene regulation (PTR) such as RNA-binding proteins (RBP) and microRNAs identified several of these factors as being crucially involved in controlling the expression of chemokines upon airway epithelial cell stimulation with cytokines prototypic of Th1-or Th2-driven responses. These studies also uncovered the participation of these pathways to glucocorticoids' inhibitory effect on the epithelial chemokine network. Unmasking the molecular mechanisms of chemokine PTR may likely uncover novel therapeutic strategies for the blockade of proinflammatory pathways that are pathogenetic for asthma, COPD, and other lung inflammatory diseases.

UR - http://www.scopus.com/inward/record.url?scp=84898731026&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84898731026&partnerID=8YFLogxK

U2 - 10.1089/jir.2013.0149

DO - 10.1089/jir.2013.0149

M3 - Article

C2 - 24697203

AN - SCOPUS:84898731026

VL - 34

SP - 255

EP - 266

JO - Journal of Interferon and Cytokine Research

JF - Journal of Interferon and Cytokine Research

SN - 1079-9907

IS - 4

ER -