TY - JOUR
T1 - Chorionic gonadotropin alleviates thioglycollate-induced peritonitis by affecting macrophage function
AU - Wan, H
AU - Coppens, Jojanneke
AU - Van Helden - Meeuwsen, Corine
AU - Leenen, Pieter
AU - van Rooijen, N
AU - Khan, Nisar
AU - Kiekens, RCM (Rebecca)
AU - Benner, Rob
AU - Versnel, Marjan
PY - 2009
Y1 - 2009
N2 - Human chorionic gonadotrophin (hCG) is a hormone produced during pregnancy and present at the implantation site and in the maternal blood. Pregnancy has been proposed to represent a controlled state of inflammation at an early stage at the implantation site and later, systemically extended to the maternal circulation. Earlier, we reported that hCG can inhibit the development of diabetes in NOD mice and LPS-induced septic shock in a murine model. We hypothesize that hCG can contribute to the reduction of inflammation by modifying M phi function. Here, the TG-induced peritonitis model for inflammation was used to investigate the effect of hCG on cytokine production and cell recruitment in vivo. hCG pretreatment in TG-induced peritonitis increased the number of peritoneal cells, especially PMN and monocytes, compared with mice injected with TG only. This increased cell number was partially explained by increased cell survival induced by hCG. Despite the cellular infiltrate, hCG pretreatment decreased i.p. TNF-alpha, IL-6, PTX3, CCL3, and CCL5 levels. By depleting peritoneal resident M phi using clodronate liposomes prior to the application of hCG and the TG trigger, we established that M phi are the main responsive cells to hCG, as the suppressed TNF-alpha and IL-6 production and increased PMN influx are abolished in their absence. Together, these data suggest that hCG contributes to the controlled inflammatory state of pregnancy by regulating M phi proinflammatory function. J. Leukoc. Biol. 86: 361-370; 2009.
AB - Human chorionic gonadotrophin (hCG) is a hormone produced during pregnancy and present at the implantation site and in the maternal blood. Pregnancy has been proposed to represent a controlled state of inflammation at an early stage at the implantation site and later, systemically extended to the maternal circulation. Earlier, we reported that hCG can inhibit the development of diabetes in NOD mice and LPS-induced septic shock in a murine model. We hypothesize that hCG can contribute to the reduction of inflammation by modifying M phi function. Here, the TG-induced peritonitis model for inflammation was used to investigate the effect of hCG on cytokine production and cell recruitment in vivo. hCG pretreatment in TG-induced peritonitis increased the number of peritoneal cells, especially PMN and monocytes, compared with mice injected with TG only. This increased cell number was partially explained by increased cell survival induced by hCG. Despite the cellular infiltrate, hCG pretreatment decreased i.p. TNF-alpha, IL-6, PTX3, CCL3, and CCL5 levels. By depleting peritoneal resident M phi using clodronate liposomes prior to the application of hCG and the TG trigger, we established that M phi are the main responsive cells to hCG, as the suppressed TNF-alpha and IL-6 production and increased PMN influx are abolished in their absence. Together, these data suggest that hCG contributes to the controlled inflammatory state of pregnancy by regulating M phi proinflammatory function. J. Leukoc. Biol. 86: 361-370; 2009.
U2 - 10.1189/jlb.0208126
DO - 10.1189/jlb.0208126
M3 - Article
C2 - 19414540
SN - 0741-5400
VL - 86
SP - 361
EP - 370
JO - Journal of Leukocyte Biology
JF - Journal of Leukocyte Biology
IS - 2
ER -