RGD Reference Report - Macrophage derived chemokine (CCL22), thymus and activation-regulated chemokine (CCL17), and CCR4 in idiopathic pulmonary fibrosis. - Rat Genome Database

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Macrophage derived chemokine (CCL22), thymus and activation-regulated chemokine (CCL17), and CCR4 in idiopathic pulmonary fibrosis.

Authors: Yogo, Y  Fujishima, S  Inoue, T  Saito, F  Shiomi, T  Yamaguchi, K  Ishizaka, A 
Citation: Yogo Y, etal., Respir Res. 2009 Aug 29;10:80.
RGD ID: 4145488
Pubmed: PMID:19715610   (View Abstract at PubMed)
PMCID: PMC2741459   (View Article at PubMed Central)
DOI: DOI:10.1186/1465-9921-10-80   (Journal Full-text)

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a chronically progressive interstitial lung disease of unknown etiology. Previously, we have demonstrated the selective upregulation of the macrophage-derived chemokine CCL22 and the thymus activation-regulated chemokine CCL17 among chemokines, in a rat model of radiation pneumonitis/pulmonary fibrosis and preliminarily observed an increase in bronchoalveolar (BAL) fluid CCL22 levels of IPF patients. METHODS: We examined the expression of CCR4, a specific receptor for CCL22 and CCL17, in bronchoalveolar lavage (BAL) fluid cells, as well as the levels of CCL22 and CCL17, to elucidate their pathophysiological roles in pulmonary fibrosis. We also studied their immunohistochemical localization. RESULTS: BAL fluid CCL22 and CCL17 levels were significantly higher in patients with IPF than those with collagen vascular diseases and healthy volunteers, and there was a significant correlation between the levels of CCL22 and CCL17 in patients with IPF. CCL22 levels in the BAL fluid did not correlate with the total cell numbers, alveolar lymphocytes, or macrophages in BAL fluid. However, the CCL22 levels significantly correlated with the numbers of CCR4-expressing alveolar macrophages. By immunohistochemical and immunofluorescence analysis, localization of CCL22 and CCR4 to CD68-positive alveolar macrophages as well as that of CCL17 to hyperplastic epithelial cells were shown. Clinically, CCL22 BAL fluid levels inversely correlated with DLco/VA values in IPF patients. CONCLUSION: We speculated that locally overexpressed CCL22 may induce lung dysfunction through recruitment and activation of CCR4-positive alveolar macrophages.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CCL17Humanpulmonary fibrosis  IEP protein:increased expression:respiratory system fluid/secretionRGD 
CCL22Humanpulmonary fibrosis  IEP protein:increased expression:respiratory system fluid/secretionRGD 
Ccl17Ratpulmonary fibrosis  ISOCCL17 (Homo sapiens)protein:increased expression:respiratory system fluid/secretionRGD 
Ccl17Mousepulmonary fibrosis  ISOCCL17 (Homo sapiens)protein:increased expression:respiratory system fluid/secretionRGD 
Ccl22Ratpulmonary fibrosis  ISOCCL22 (Homo sapiens)protein:increased expression:respiratory system fluid/secretionRGD 
Ccl22Mousepulmonary fibrosis  ISOCCL22 (Homo sapiens)protein:increased expression:respiratory system fluid/secretionRGD 

Objects Annotated

Genes (Rattus norvegicus)
Ccl17  (C-C motif chemokine ligand 17)
Ccl22  (C-C motif chemokine ligand 22)

Genes (Mus musculus)
Ccl17  (C-C motif chemokine ligand 17)
Ccl22  (C-C motif chemokine ligand 22)

Genes (Homo sapiens)
CCL17  (C-C motif chemokine ligand 17)
CCL22  (C-C motif chemokine ligand 22)


Additional Information