Eosinophil apoptosis induced by fungal immunomodulatory peptide-fve via reducing IL-5alpha receptor.
OBJECTIVE
Eosinophils are important effector cells in the pathogenesis of allergic bronchial asthma. Enhancement of eosinophil apoptosis has been considered to have therapeutic effect on allergic disease. Fungal immunomodulatory peptide (FIP)-fve has been reported to possess immunoprophylactic activities for allergic diseases. The purpose of this study was to investigate the modulation of FIP-fve on human eosinophil survival derived from allergic asthmatic patients.


METHODS
Eosinophils were obtained from allergic asthmatic patients and purified with the use of density gradients and immunomagnetic beads negative selection. Apoptosis was assessed by annexin V and propidium iodide. The apoptotic signal protein, CD95 and IL-5 receptor expression were assessed by Western blot and flow cytometric analysis.


RESULTS
When the eosinophils were treated with FIP-fve in the presence of IL-5, IL-5-enhanced eosinophil survival diminished. FIP-fve could reduce IL-5-mediated survival of eosinophils and decrease IL-5Ralpha expression. In the presence of FIP-fve, CD95 expression was upregulated and Bcl-xL and pro-caspase 3 expression were downregulated in cultured eosinophils.


CONCLUSIONS
The results suggest that FIP-fve can inhibit IL-5-mediated survival of eosinophils through the modulation of cytokine receptor expression and apoptotic signal protein production. The modulatory effect of FIP-fve on eosinophil apoptosis in vitro indicates that it may have some therapeutic effect on eosinophil-related allergic inflammation in vivo.
Hsieh
Chia-Wei
CW
Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.
Lan
Joung-Liang
JL
Meng
Qiu
Q
Cheng
Ya-Wen
YW
Huang
Huei-Mei
HM
Tsai
Jaw-Ji
JJ
D017209:Apoptosis / Q000187:drug effects*; D001249:Asthma / Q000276:immunology; D015153:Blotting, Western; D053148:Caspase 3 / Q000378:metabolism; D004804:Eosinophils / Q000187:drug effects* / Q000276:immunology; D005434:Flow Cytometry; D005656:Fungal Proteins / Q000494:pharmacology*; D006801:Humans; D015848:Interleukin-5 / Q000494:pharmacology*; D053649:Receptors, Interleukin-5 / Q000378:metabolism; D015398:Signal Transduction; D051020:bcl-X Protein / Q000378:metabolism
C494811:BCL2L1 protein, human; D005656:Fungal Proteins; D015848:Interleukin-5; D053649:Receptors, Interleukin-5; D051020:bcl-X Protein; D053148:Caspase 3