Open AccessIL‐5 but not interferon‐gamma (IFN‐γ) inhibits eosinophil apoptosis by up‐regulation of bcl‐2 expression
Author(s) -
OCHIAI K.,
KAGAMI M.,
MATSUMURA R.,
TOMIOKA H.
Publication year - 1997
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.1997.d01-884.x
Subject(s) - eosinophil , apoptosis , microbiology and biotechnology , in vitro , biology , eosinophil cationic protein , messenger rna , immunology , interferon gamma , biochemistry , gene , asthma
In order to determine regulatory mechanisms of eosinophil apoptosis, we examined the effect of recombinant IL‐5 and interferon‐gamma (IFN‐γ) on eosinophil apoptosis and bcl‐2 expression. rhIL‐5 (2.5 ng/ml) significantly inhibited eosinophil apoptosis in 96 h in vitro culture compared with medium only‐cultured eosinophils (89.4 ± 3.6% versus 31.3 ± 12.2% (mean ± s.d.); n = 7, P < 0.05). Further, rhIL‐5 significantly increased bcl‐2 protein and mRNA expression on cultured eosinophils. A phosphorothioate antisense oligonucleotide targeted at the ATG translation initiation codon of bcl‐2 (10 −5 m ) could significantly block the supportive effect of rhIL‐5 (0.25 ng/ml) for eosinophil survival compared with sense cDNA of bcl‐2 on 96 h culture (inhibition rate 28.01 ± 4.56% versus 0.07 ± 1.73%; n = 4, P < 0.05). In contrast, rhIFN‐γ (100 U/ml) significantly inhibited eosinophil apoptosis on 96 h in vitro culture (72.7 ± 10.5%; n = 7, P < 0.05), but did not significantly up‐regulate bcl‐2 protein and mRNA. These results indicate that IL‐5 has inhibitory effects on eosinophil apoptosis by regulation of bcl‐2 expression.