To the Editor:
In their report, Dibbert et al1 had described that spontaneous eosinophil apoptosis was associated with a decrease in the levels of the antiapoptotic Bcl-XL protein. Because they also observed that granulocyte-macrophage colony-stimulating factor or interleukin-5 could maintain Bcl-XL mRNA and protein levels, they postulated that these cytokines may use Bcl-XLto prevent spontaneous eosinophil apoptosis. To determine whether this is true, they had used “Bcl-XL antisense oligonucleotides (oligos)” to inhibit Bcl-XL protein expression and studied the effects of Bcl-XL protein inhibition on eosinophil apoptosis. The sequence of their Bcl-XL antisense oligos is 5′-TGT ATC CTT TCT GGG AAA GC-3′. This sequence binds to nucleotides 182 to 191 in the Bcl-XL gene2: GCT TTC CCA GAA AGG ATA CA. However, this sequence is also identical to nucleotides 182 to 191 in the Bcl-XS gene.2 Therefore, this antisense sequence is mislabeled; it should not be named as Bcl-XLantisense but instead as Bcl-X antisense because it binds to both Bcl-XL and Bcl-XS mRNA. Since the investigators showed that only Bcl-XL, but not Bcl-XS, mRNA is expressed in freshly purified eosinophils, their studies with the Bcl-X antisense are probably still valid. However, if others want to use this antisense sequence to study Bcl-XL function, they need to be very careful, especially if Bcl-XS protein is also expressed in their system. In that case, perhaps another Bcl-XL antisense oligo may be more appropriate.
Response
We agree with the comments of Dr Tari on our recently published work.1 The used antisense oligodeoxynucleotides would probably also decrease Bcl-xs levels in cells, which express Bcl-xs, and should then be called Bcl-x antisense. However, eosinophils did not express Bcl-xs under all conditions mentioned in our report. Therefore, in the system used, the oligodeoxynucleotides were real Bcl-xL antisense molecules.
