李氏杆菌病和孕期的其他细菌感染会影响胎儿及母亲，但对于病原体是怎样穿过胎盘障碍的人们却知之甚少。
Disson等人利用被Listeria monocytogenes感染的两个互补动物模型对这一过程进行了研究。
他们发现，病原体向胎盘的转移同时需要两个毒性因子或入侵蛋白，即InlA 和 InlB。所以阻断这两个通道中的一个或将其全部阻断，有可能阻止细菌进入胎儿体内。反过来说，人们也许有可能利用这两个通道来输送穿过同一障碍的治疗用分子。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature 455, 1114-1118 (23 October 2008) | doi:10.1038/nature07303
Conjugated action of two species-specific invasion proteins for fetoplacental listeriosis
Olivier Disson1,2,10, Solène Grayo1,2,3,10, Eugénie Huillet4,5,6,10, Georgios Nikitas1,2, Francina Langa-Vives7, Olivier Dussurget4,5,6, Marie Ragon3, Alban Le Monnier3, Charles Babinet8,11, Pascale Cossart4,5,6 & Marc Lecuit1,2,3,9
1 Institut Pasteur, Groupe Microorganismes et Barrières de l'H?te, Unité des Interactions Bactéries-Cellules, F-75015 Paris, France
2 Inserm Avenir U604, F-75015 Paris, France
3 Institut Pasteur, Centre National de Référence des Listeria, F-75015 Paris, France
4 Institut Pasteur, Unité des Interactions Bactéries-Cellules, F-75015 Paris, France
5 Inserm U604, F-75015 Paris, France
6 INRA USC2020, F-75015 Paris, France
7 Institut Pasteur, Centre d'Ingénierie Génétique Murine, F-75015 Paris, France
8 Institut Pasteur, Unité de Biologie du Développement, F-75015 Paris, France
9 Centre d'Infectiologie Necker-Pasteur, Service des Maladies Infectieuses et Tropicales, H?pital Necker-Enfants malades, Assistance Publique-H?pitaux de Paris, Université Paris Descartes, F-75015 Paris, France
The ability to cross host barriers is an essential virulence determinant of invasive microbial pathogens. Listeria monocytogenes is a model microorganism that crosses human intestinal and placental barriers, and causes severe maternofetal infections by an unknown mechanism1. Several studies have helped to characterize the bacterial invasion proteins InlA and InlB2. However, their respective species specificity has complicated investigations on their in vivo role3, 4. Here we describe two novel and complementary animal models for human listeriosis: the gerbil, a natural host for L. monocytogenes, and a knock-in mouse line ubiquitously expressing humanized E-cadherin. Using these two models, we uncover the essential and interdependent roles of InlA and InlB in fetoplacental listeriosis, and thereby decipher the molecular mechanism underlying the ability of a microbe to target and cross the placental barrier.
