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Metabolic Glycoengineering of Sialic Acid Using N-acyl-modified Mannosamines
Published on: November 25, 2017
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Sialic acid is a critical fetal defense against maternal complement attack
Markus Abeln1, Iris Albers1, Ulrike Peters-Bernard1
1Institut for Clinical Biochemistry and.
The Journal of Clinical Investigation
|November 2, 2018
Summary
Sialic acid (Sia) is crucial for protecting pregnant mice from immune attack. Its absence causes developmental failure by activating complement and impairing placental development, leading to embryonic lethality.
Area of Science:
- Immunology
- Developmental Biology
- Glycobiology
Background:
- Sialic acid (Sia) is a negatively charged sugar found on cell surface glycans.
- Genetic ablation of CMP-sialic acid synthase (CMAS) leads to a lack of sialylated glycans.
Purpose of the Study:
- To investigate the role of sialic acid (Sia) in embryonic development and fetal-maternal immune homeostasis.
- To understand the mechanisms underlying embryonic lethality in Cmas-/- mice.
Main Methods:
- Genetic ablation of CMP-sialic acid synthase (CMAS) in mice.
- Analysis of embryonic development, placental morphology, and immune cell infiltration.
- Complement system manipulation using cobra venom factor.
Main Results:
- Lack of sialic acid (Sia) in Cmas-/- mice caused embryonic lethality by E9.5 due to complement activation on trophoblasts.
- Phenotype included maternal neutrophil infiltration, intrauterine growth restriction, and impaired placental development.
- Complement depletion rescued the embryonic lethality, highlighting Sia's role in immune protection.
Conclusions:
- Sialic acid (Sia) is dispensable for early embryonic development but essential for fetal-maternal immune homeostasis.
- Sia protects the allograft implant from maternal innate immune attack.
- Impaired placentation and subsequent malnutrition are secondary effects of sialylation deficiency.
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