Heat Shock Proteins and Heat Shock Protein-Antibody Complexes in Placental Tissues. Issue 4 (1999)

• Record Type: Journal Article
• Authors: Ziegert, M.; Witkin, S. S.; Sziller, I.; Alexander, H.; Brylla, E.; Härtig, W.
• Is Part Of: Infectious diseases in obstetrics and gynecology. Volume 7:Issue 4(1999)
• Page Start: 180
• Page End: 185
• Publication Date: 1999
• Subjects: Generative organs, Female -- Infections -- Periodicals; Communicable diseases in pregnancy -- Periodicals; 618.142005
• DOI: 10.1155/S1064744999000307
• Languages: English
• ISSNs: 1064-7449

Abstract

Abstract : Objective: The relationship between pregnancy outcome and expression of the heat shock proteins (hsps) or hsp-antibody complexes of 60kD (hsp60), 70kD (hsp70), and 90kD (hsp90) in placental tissue and circulating antibodies to hsps was evaluated. Method: Expression of hsp60, hsp70, and hsp90 in placentae from 12 women with preterm birth, eight with intrauterine growth restriction (IUGR), and 10 with term birth, as well as the presence of the corresponding antibodies, was investigated by a new carbocyanine double fluorescence technique. Results were compared with microbiological findings and circulating antibodies to hsps in sera. Results: In each placental specimen examined, hsp60, hsp70, and hsp90 were identified. However, hsp70-antibody complexes were detected in only four of the preterm labor cases. Similarly, hsp60-antibody complexes were detected in only five preterm labor patients and in one patient with IUGR. None of the placentae contained hsp90-antibody complexes. In the preterm birth group, all patients with hsp60-antibody complexes were also positive for circulating antibodies to hsp60. The presence of hsp70-antibody complexes also correlated with hsp70 antibody in sera. Conclusions: Formation of hsp60- and hsp70-antibody complexes in the placenta may contribute to the induction of preterm birth. Women sensitized to these antibodies may be at increased risk for adverse pregnancy outcome. Infect. Dis. Obstet. Gynecol. 7:180–185, 1999.