PROBLEM: To give an approach in order to elucidate the mechanism by which p
lacental IL-6 induce modifications in the glycosylation status of immunoglo
bulins, in the present work, we investigate a putative relationship between
a stimulus by placental IL-6 and expression of cytoplasmic "hsp70 family p
roteins" in an in vitro model.
METHODS OF STUDY: Supernatants of cultures of placentae obtained from primi
parous and multiparous AKR/J x AKR/J and AKR/J x BALB/c mouse crossbreeding
s were added to mouse IgG1 hybridoma cultures which produced symmetric and
asymmetric anti-dinitrophenol (anti-DNP) antibodies. Analyses of the expres
sion of inducible hsp72/constitutive hsp73 in cellular lysates obtained fro
m hybridomas cultured, in the presence of rmIL-6 or crude murine placental
culture supernatants; followed by neutralization assays with anti IL-6, wer
e performed. In addition, the level of IL-6 present in the employed placent
al culture supernatants was determined and compared with the placental hsp7
RESULTS: These experiments showed that mouse placentae were able to release
IL-6 in vitro. In addition, mouse placental supernatants (PS) containing o
ver 1,000 pg/mL of IL-6 enhanced the expression of the inducible isoform hs
p72 in the employed hybridomas. This effect was abolished when the hsp70-in
ducing PS were previously incubated with anti-mIL6 antibody.
CONCLUSIONS: These observations indicate that mouse placentae produce diffe
rent titers of IL-6 and suggest that IL-6 appears to be the unique mouse pl
acental factor able to induce in vitro hsp72 synthesis. A relationship with
the increased synthesis of anti-paternal antigen asymmetric antibodies, pr
eviously observed during pregnancy, is discussed.