1. Activation of the IL-1β/CXCL1/MMP-10 axis in chorioamnionitis induced by inactivated Group B Streptococcus
- Author
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Djordje Grbic, Louis-Charles Fortier, Cathy Vaillancourt, Noha Gerges, Marie-Julie Allard, Julie Bergeron, Clémence Guiraut, Guillaume Sébire, Université de Sherbrooke (UdeS), McGill University = Université McGill [Montréal, Canada], Institut Armand Frappier (INRS-IAF), and Institut National de la Recherche Scientifique [Québec] (INRS)-Réseau International des Instituts Pasteur (RIIP)
- Subjects
Group B Streptococcus ,0301 basic medicine ,Chemokine ,Chemokine CXCL1 ,Placenta ,[SDV]Life Sciences [q-bio] ,Interleukin-1beta ,Inflammation ,Biology ,Chorioamnionitis ,03 medical and health sciences ,Matrix Metalloproteinase 10 ,Pregnancy ,Streptococcal Infections ,Maternal immune activation ,medicine ,Animals ,reproductive and urinary physiology ,Fetus ,Innate immune system ,Streptococcus ,Obstetrics and Gynecology ,Interleukin ,medicine.disease ,Interleukin-1β ,Rats ,3. Good health ,CXCL1 ,Disease Models, Animal ,030104 developmental biology ,medicine.anatomical_structure ,Reproductive Medicine ,Immunology ,biology.protein ,Female ,medicine.symptom ,Developmental Biology - Abstract
International audience; 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)-1β has a major role in anti-GBS host defense, we hypothesized that IL-1β-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-1β hyper expression. Following placental chemokine (C-X-C motif) ligand 1 (CXCL1) production, polymorphonuclear leukocytes (PMN) placental infiltration started at 24 h 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-1β 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.
- Published
- 2016
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