EP4 and EP2 receptor activation of protein kinase A by prostaglandin E2 impairs macrophage phagocytosis of Clostridium sordellii.
Am J Reprod Immunol
; 71(1): 34-43, 2014 Jan.
Article
en En
| MEDLINE
| ID: mdl-23902376
ABSTRACT
PROBLEM:
Clostridium sordellii causes endometrial infections, but little is known regarding host defenses against this pathogen. METHOD OF STUDY We tested the hypothesis that the immunoregulatory lipid prostaglandin (PG) E2 suppresses human macrophage clearance of C. sordellii through receptor-induced increases in intracellular cyclic adenosine monophosphate (cAMP). The THP-1 macrophage cell line was used to quantify C. sordellii phagocytosis.RESULTS:
PGE2 increased cAMP levels, activated protein kinase A (PKA), and inhibited the class A scavenger receptor-dependent phagocytosis of C. sordellii. Activation of the EP2 and EP4 receptors increased intracellular cAMP and inhibited phagocytosis, with evidence favoring a more important role for EP4 over EP2. This was supported by EP receptor expression data and the use of pharmacological receptor antagonists. In addition, the PKA isoform RI appeared to be more important than RII in mediating the suppression of ingestion of C. sordellii.CONCLUSION:
The endogenous lipid mediator PGE2 impairs human innate immune responses against C. sordellii.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Infecciones por Clostridium
/
Clostridium sordellii
/
Subtipo EP2 de Receptores de Prostaglandina E
/
Subtipo EP4 de Receptores de Prostaglandina E
/
Macrófagos
Límite:
Humans
Idioma:
En
Revista:
Am J Reprod Immunol
Año:
2014
Tipo del documento:
Article
País de afiliación:
Estados Unidos