[Inhibitory effects of Galectin-3 on the inflammatory cytokines and chemokines in guinea pig asthma models].
OBJECTIVE
To elucidate the roles of interleukin-5 (IL-5), Eotaxin, and CCR-3 in eosinophilic inflammation in guinea pig asthma models and investigate the inhibitory effects of Galectin-3.


METHODS
Thirty-two guinea pigs were randomly assigned to control group, asthma group, Galectin-3 intervention group, and dexamethasone (DXM) intervention group. Asthma models were established by sensitizing-challenging the animals with ovalbumin(OVA). The asthmatic animals were treated with Galectin-3 at 0.5 mg/kg, or DXM at 1 mg/kg, respectively,by peritoneally injection one hour before each aerosol challenge from the 14th day to 16th day after sensitization while the control animals were treated with normal saline. The specimens of peripheral blood, bone marrow, and lung tissue on slides were prepared respectively and stained with HE. Then the total number and percentage of eosinophils (EOS) were counted. The lung tissue slide was stained immunochemically with anti-IL-5 polyclonal antibody, anti-Eotaxin polyclonal antibody, and anti-CCR-3 polyclonal antibody, respectively. The immunoactive cells were counted and represented as percentages in total cells.


RESULTS
The amounts of EOS in peripheral blood, bone marrow,and lung tissue as well as percentages of IL-5, Eotaxin,and CCR-3 immunoactive cells in the lung tissue from asthma group were increased significantly, compared to those from control group. DXM significantly decreased the amounts of EOS, percentages of IL-5, Eotaxin, and CCR-3 immunoactive cells (P < 0.05). Galectin-3 had an equivalent suppressive effects on the amounts of EOS and IL-5+ cells with DXM (P > 0.05) and down-regulated CCR-3 expression (P < 0.05) to a less extent when compared to DXM (P < 0.05), but had minimal effect on Eotaxin expression (P > 0.05).


CONCLUSIONS
This study provides further evidence for an eosinophil recruitment from bone marrow to circulation blood to lung in asthmatic response, in which overexpression of IL-5, Eotaxin, and CCR-3 could be involved. Galectin-3, a selective inhibitor of IL-5 mRNA transcription, might potentially suppress eosinophilc inflammation and be a compromising specific anti-asthma reagent.
Li
Lian
L
Department of Respiratory Diseases, West China Hospital, Sichuan University, Chengdu, China.
Liu
Chun-tao
CT
Wang
Ke
K
Pang
Ya-min
YM
D000818:Animals; D001249:Asthma / Q000378:metabolism*; D002452:Cell Count; D054413:Chemokine CCL11; D018925:Chemokines / Q000378:metabolism; D019742:Chemokines, CC / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology; D004804:Eosinophils; D005260:Female; D037502:Galectin 3 / Q000494:pharmacology*; D006168:Guinea Pigs; D015848:Interleukin-5 / Q000378:metabolism; D008168:Lung / Q000378:metabolism; D008297:Male; D011897:Random Allocation; D054397:Receptors, CCR3; D019707:Receptors, Chemokine / Q000096:biosynthesis* / Q000235:genetics
D054413:Chemokine CCL11; D018925:Chemokines; D019742:Chemokines, CC; D037502:Galectin 3; D015848:Interleukin-5; D054397:Receptors, CCR3; D019707:Receptors, Chemokine; D003907:Dexamethasone