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

Bergeron, Julie; Gerges, Noha; Guiraut, Clémence; Grbic, Djordje; Allard, Marie-Julie; Fortier, Louis-Charles; Vaillancourt, Cathy; Sebire, Guillaume (2016). Activation of the IL-1β/CXCL1/MMP-10 axis in chorioamnionitis induced by inactivated Group B Streptococcus Placenta , vol. 47 . p. 116-123. DOI: 10.1016/j.placenta.2016.09.016.

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Résumé

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)-1beta has a major role in anti-GBS host defense, we hypothesized that IL-1beta-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-1beta 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-1beta 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.

Type de document: Article
Mots-clés libres: Chorioamnionitis; Maternal immune activation; Group B; Streptococcus; Placenta; Inflammation; Interleukin-1β
Centre: Centre INRS-Institut Armand Frappier
Date de dépôt: 26 mars 2019 05:07
Dernière modification: 26 mars 2019 05:07
URI: http://espace.inrs.ca/id/eprint/6704

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