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CpG Oligodeoxynucleotides Downregulate Placental Adiponectin and Increase Embryo Loss in Non-Obese Diabetic Mice
Chuan-Mei Qin1, Fu-Ju Tian1, Xiao-Rui Liu1
1Institute of Embryo-Fetal Original Adult Disease, The International Peace Maternity & Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Problem:
CpG oligodeoxynucleotides (ODNs) can induce immunological changes in non-obese diabetic (NOD) mice and increase embryo loss, but little is known about the mechanism. This study aimed to determine the role of adiponectin in CpG ODN-induced pregnancy failure.
Method Of Study:
Oligodeoxynucleotide 1826 was intraperitoneally injected to NOD mice, and ODN 2216, ODN 2006, and ODN 2395 were used to stimulate human trophoblast cell lines to investigate adiponectin expression patterns and its possible effects on trophoblast function.
Results:
CpG ODNs downregulated adiponectin via the cJun N-terminal kinase signaling pathway and led to increased embryo loss (from 6.9 to 33.3%). ODN 2006 impaired human trophoblast cell migration, which was successfully rescued by adiponectin treatment.
Conclusion:
CpG ODNs decreased placental adiponectin expression in NOD mice and impaired human trophoblast function and was associated with increased embryo loss. Adiponectin may therefore play an important protective role in the prevention of bacteria-induced pregnancy failure.
Insights
CpG oligodeoxynucleotides (ODNs) reduce adiponectin, a protective protein, leading to increased embryo loss in mice. Adiponectin treatment rescued impaired trophoblast cell function, suggesting its vital role in preventing pregnancy failure.
Area of Science:
- Immunology
- Reproductive Biology
- Endocrinology
Background:
- CpG oligodeoxynucleotides (ODNs) can cause immunological changes and embryo loss in non-obese diabetic (NOD) mice.
- The precise mechanisms underlying CpG ODN-induced pregnancy failure remain largely unknown.
Purpose of the Study:
- To investigate the role of adiponectin in CpG ODN-induced pregnancy failure.
- To determine how CpG ODNs affect adiponectin expression and trophoblast function.
Main Methods:
- CpG ODN 1826 was administered to NOD mice.
- Human trophoblast cell lines were stimulated with CpG ODNs (2216, 2006, 2395) to assess adiponectin expression and trophoblast function.
Main Results:
- CpG ODNs downregulated adiponectin through the cJun N-terminal kinase pathway, significantly increasing embryo loss from 6.9% to 33.3%.
- CpG ODN 2006 impaired human trophoblast cell migration, an effect reversed by adiponectin treatment.
Conclusions:
- CpG ODNs reduce placental adiponectin in NOD mice, impairing trophoblast function and correlating with increased embryo loss.
- Adiponectin appears to play a crucial protective role in preventing pregnancy failure potentially induced by bacterial components.
