caa a22 4500 44588486X CHVBK 20180317145556.0 cr unu---uuuuu 170323e20110101xx s 000 0 eng 10.1007/s00011-010-0241-1 doi (NATIONALLICENCE)springer-10.1007/s00011-010-0241-1 The macrophage pattern recognition scavenger receptors SR-A and CD36 protect against microbial induced pregnancy loss [Elektronische Daten] [Helieh Oz, Jeffery Ebersole, Willem de Villiers] 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 1week. 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) 24-74h 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. Springer Basel AG, 2010 Reproductive loss nationallicence Gut permeability nationallicence Streptococcus nationallicence Actinobacillus nationallicence SR-A/CD36−/−mice nationallicence Oz Helieh Center for Oral Health Research, MN310 College of Dentistry and Internal Medicine, University of Kentucky Medical Center, 800 Rose Street, 40536, Lexington, KY, USA aut Ebersole Jeffery Center for Oral Health Research, MN310 College of Dentistry and Internal Medicine, University of Kentucky Medical Center, 800 Rose Street, 40536, Lexington, KY, USA aut de Villiers Willem Division of Digestive Diseases and Nutrition, Department of Internal Medicine, University of Kentucky Medical Center, Lexington, KY, USA aut Inflammation Research SP Birkhäuser Verlag Basel 60/1(2011-01-01), 93-97 1023-3830 60:1<93 2011 60 11 https://doi.org/10.1007/s00011-010-0241-1 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00011-010-0241-1 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Oz Helieh Center for Oral Health Research, MN310 College of Dentistry and Internal Medicine, University of Kentucky Medical Center, 800 Rose Street, 40536, Lexington, KY, USA aut NATIONALLICENCE 700 1- Ebersole Jeffery Center for Oral Health Research, MN310 College of Dentistry and Internal Medicine, University of Kentucky Medical Center, 800 Rose Street, 40536, Lexington, KY, USA aut NATIONALLICENCE 700 1- de Villiers Willem Division of Digestive Diseases and Nutrition, Department of Internal Medicine, University of Kentucky Medical Center, Lexington, KY, USA aut NATIONALLICENCE 773 0- Inflammation Research SP Birkhäuser Verlag Basel 60/1(2011-01-01), 93-97 1023-3830 60:1<93 2011 60 11 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer