Involvement of galectin-9 in lung eosinophilia in patients with eosinophilic pneumonia.
BACKGROUND
Although we first found galectin-9 (Gal-9) as an eosinophil chemoattractant, its role in eosinophilic inflammation is still obscure. The purpose of the present study is to clarify the role of Gal-9 in human eosinophilic pulmonary inflammation in comparison with eotaxin (CCL11).


METHODS
We measured the levels of Gal-9 and eotaxin in the bronchoalveolar lavage fluid (BALF) of patients with acute and chronic eosinophilic pneumonia (AEP and CEP). Furthermore, the biological activities (chemotaxis and apoptosis) of Gal-9 were compared with those of eotaxin using interleukin-5-primed or -unprimed eosinophils.


RESULTS
The levels of Gal-9 and eotaxin in the BALF from patients with AEP and those with CEP were higher than those found in the controls. Although there was little difference in Gal-9 level between patients with AEP and patients with CEP, the eotaxin level was significantly lower in patients with CEP. In patients with AEP, the eosinophil number correlated well with both the Gal-9 and eotaxin levels. However, in patients with CEP, the eosinophil number only correlated well with the Gal-9 level. Moreover, the Gal-9 level correlated with the eotaxin level in patients with AEP, but there was no significant correlation between those levels in patients with CEP. Anti-Gal-9 antibody treatment strongly reduces eosinophil chemotactic activity in the BALF of patients with AEP and in that of patients with CEP, whereas the anti-CCR3 (receptor for eotaxin) antibody strongly reduces this activity in the BALF of patients with AEP but not in that of patients with CEP. Furthermore, Gal-9 exhibited both chemotactic and proapoptotic activities for activated eosinophils, though eotaxin only exhibited chemotactic activity.


CONCLUSIONS
The present results provide two possibilities: that Gal-9 is involved in pulmonary eosinophilia in patients with AEP and CEP, and that Gal-9 exhibits regulatory functions for activated eosinophils at the site of inflammation.
Katoh
Shigeki
S
Department of Cell Regulation, Faculty of Medicine, Kagawa University, Kagawa, Japan. kshigeki@med.kagawa-u.ac.jp
Nobumoto
Atsuya
A
Matsumoto
Nobuhiro
N
Matsumoto
Kiyoshi
K
Ehara
Naomi
N
Niki
Toshiro
T
Inada
Hiroyuki
H
Nishi
Nozomu
N
Yamauchi
Akira
A
Fukushima
Kiyoyasu
K
Hirashima
Mitsuomi
M
D054413:Chemokine CCL11 / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000166:cytology; D005260:Female; D037161:Galectins / Q000276:immunology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011014:Pneumonia / Q000276:immunology / Q000503:physiopathology*; D011657:Pulmonary Eosinophilia / Q000276:immunology / Q000503:physiopathology*
D054413:Chemokine CCL11; D037161:Galectins; C105032:LGALS9 protein, human