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The macrophage pattern recognition scavenger receptors SR-A and CD36 protect against microbial induced pregnancy loss
Helieh S Oz1, Jeffery L Ebersole, Willem J S de Villiers
1Center for Oral Health Research, MN310 College of Dentistry and Internal Medicine, University of Kentucky Medical Center, 800 Rose Street, Lexington, KY 40536, USA. Helieh.oz@uky.edu
Objectives And Design:
Microbial products can act via stress-induced signaling cascades to link dysregulated endogenous microbiota to immune activation (e.g., macrophages) and pregnancy loss. Our previous studies demonstrated that mice deficient in the macrophage pattern recognition scavenger receptors, SR-A and CD36, are more susceptible to inflammatory complications including gut leakiness and experimental colitis. We hypothesized that bacterial penetration of the maternal mucosal surfaces and replication in embryonic fluids compromise the fetal status and can result in miscarriage.
Materials And Methods:
Eighty pregnant ICR and SR-A/CD36-deficient mice were injected via tail vein or intraperitoneally with commensal bacteria (Streptococcus cricetus and/or Actinobacillus sp.) or sham controls. Dams were monitored daily for physical distress, pain and abortion.
Results:
Dams injected with single dose bacterial inoculum did not develop clinical symptoms. Day old pups injected with bacteria developed internal focal abscesses, lost weight but recovered after 1 week. Dams receiving a second bacterial inoculum delivered dead fetuses. However, SR-A/CD36-deficnet dams demonstrated 100% fetal death via aborted fetuses, and significant up-regulation of the proinflammatory markers (IL-6, serum Amyloid A) 24-74 h after single inoculum.
Conclusions:
These data indicate that macrophage scavenger receptors are required for the fetal protection against microbial attack and support that maternal transfer of innate immunity contributes to this protection.
Insights
Macrophage scavenger receptors protect fetuses from microbial attack. Deficiency in these receptors, SR-A and CD36, leads to pregnancy loss and increased inflammation during infection.
Area of Science:
- Immunology
- Reproductive Biology
- Microbiology
Background:
- Microbial products can trigger immune responses linked to pregnancy loss.
- Macrophage scavenger receptors, SR-A and CD36, are crucial for managing inflammatory responses.
- Previous studies show SR-A/CD36 deficiency increases susceptibility to inflammatory conditions.
Purpose of the Study:
- To investigate the role of macrophage scavenger receptors in protecting against microbial-induced pregnancy loss.
- To test the hypothesis that bacterial penetration compromises fetal well-being, leading to miscarriage.
Main Methods:
- Eighty pregnant mice (ICR and SR-A/CD36-deficient) were injected with commensal bacteria or sham controls.
- Mice were monitored for signs of distress, pain, and abortion.
- Pro-inflammatory markers (IL-6, serum Amyloid A) were measured.
Main Results:
- SR-A/CD36-deficient dams experienced 100% fetal death after a single bacterial inoculum.
- These deficient dams showed significant upregulation of pro-inflammatory markers.
- Multiple bacterial inoculums were required to induce fetal death in control dams.
Conclusions:
- Macrophage scavenger receptors (SR-A and CD36) are essential for protecting fetuses from microbial threats.
- Maternal innate immunity, mediated by these receptors, plays a critical role in pregnancy protection.
- Deficiency in these receptors compromises fetal survival during maternal infection.
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