Accumulation of CXCR3-expressing eosinophils and increased concentration of its ligands (IP10 and Mig) in bronchoalveolar lavage fluid of patients with chronic eosinophilic pneumonia.
BACKGROUND
Since human peripheral eosinophils have been shown to migrate to the CXC chemokine receptor 3 (CXCR3) ligands IFN-gamma-inducible protein 10 (IP10) and monokine induced by IFN-gamma (Mig), this confirms that CXCR3 is functionally expressed on these cells. IP10 expression has been shown to be increased in the airways of asthmatics. Eosinophil accumulations are found in bronchoalveolar lavage fluid (BALF) from patients with chronic eosinophilic pneumonia (CEP). To examine the contribution of IP10 and Mig in the pathogenesis of CEP, we measured the concentration of IP10 and Mig, and evaluated the expression of CXCR3 on eosinophils in BALF taken from patients with CEP.


METHODS
The concentrations of IP10 and Mig in BALF were measured by ELISA. The proportion of CXCR3-expressing CD4+ T cells and CD16-negative eosinophils was determined by flow cytometry.


RESULTS
The BALF concentrations of IP10 and Mig were higher in patients with CEP, as well as in patients with sarcoidosis, when compared to healthy controls. The absolute number of CXCR3+ CD4+ T cells was significantly higher in the BALF of patients with sarcoidosis, but not in the patients with CEP, when compared to healthy volunteers. There were higher percentages of CXCR3-expressing eosinophils in the BALF than in the peripheral blood of patients with CEP.


CONCLUSIONS
Our findings suggest that IP10 and Mig contribute to the accumulation of CXCR3-expressing eosinophils in the lungs of patients with CEP, and modulate the eosinophilic inflammation of the lung.
Katoh
Shigeki
S
Department of Cell Regulation, School of Medicine, Kagawa University, Kita-gun, Kagawa, Japan. kshigeki@med.kagawa-u.ac.jp
Fukushima
Kiyoyasu
K
Matsumoto
Nobuhiro
N
Ehara
Naomi
N
Matsumoto
Kiyoshi
K
Yamauchi
Akira
A
Hirashima
Mitsuomi
M
D000328:Adult; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry* / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D054357:Chemokine CXCL10; D054370:Chemokine CXCL9; D019743:Chemokines, CXC / Q000378:metabolism*; D002908:Chronic Disease; D004804:Eosinophils / Q000276:immunology*; D005260:Female; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism*; D008024:Ligands; D008297:Male; D008875:Middle Aged; D010361:Patients; D011014:Pneumonia / Q000276:immunology*; D011657:Pulmonary Eosinophilia / Q000276:immunology*; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine / Q000378:metabolism*; D018121:Receptors, Cytokine / Q000378:metabolism
C114753:CXCL10 protein, human; C080810:CXCL9 protein, human; C515187:CXCR3 protein, human; D054357:Chemokine CXCL10; D054370:Chemokine CXCL9; D019743:Chemokines, CXC; C104577:IP10-Mig receptor; D036341:Intercellular Signaling Peptides and Proteins; D008024:Ligands; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine; D018121:Receptors, Cytokine