Activation of the IL-1 beta/CXCL1/MMP-10 axis in chorioamnionitis induced by inactivated Group B Streptococcus

作者：Bergeron Julie; Gerges Noha; Guiraut Clemente; Grbic Djordje; Allard Marie Julie; Fortier Louis Charles; Vaillancourt Cathy; Sebire Guillaume^*

来源：Placenta, 2016, 47: 116-123.

DOI：10.1016/j.placenta.2016.09.016

• Chorioamnionitis
• Maternal immune activation
• Group B Streptococcus
• Placenta
• Inflammation
• Interleukin-1 beta

Infection or inflammation during pregnancy is known to lead to maternal immune activation triggering a fetal inflammatory response syndrome associated with deleterious effects, such as brain injury and neurodevelopmental disabilities. Group B Streptococcus (GBS) - one of the most common bacterium colonizing pregnant women - can be responsible for chorioamnionitis. Given that interleukin (IL)-1 beta has a major role in anti-GBS host defense, we hypothesized that IL-1 beta-driven innate immune response is implicated in GBS-induced chorioamnionitis. Using a rat model of GBS-induced chorioamnionitis, this study showed that inflammatory response to this pathogen was associated with maternal and placental IL-1 beta hyper expression. Following placental chemokine (C-X-C motif) ligand 1 (CXCL1) production, polymorphonuclear leukocytes (PMN) placental infiltration started at 2411 post-GBS exposure, and MMP-10 was released within these placentas. At 72 h, PMN infiltration extended to membranes and to membranes' arteries. This was associated with IL-1 beta release within the fetus blood at 72 h. Such a GBS-associated inflammatory cascade might be deleterious for fetal organs. These results pave the way toward targeted placento-protective anti-inflammatory strategies against GBS-induced chorioamnionitis.

• 出版日期2016-11
• 单位McGill