李氏桿菌病和孕期的其他細(xì)菌感染會(huì)影響胎兒及母親,，但對(duì)于病原體是怎樣穿過(guò)胎盤(pán)障礙的人們卻知之甚少,。

Disson等人利用被Listeria monocytogenes感染的兩個(gè)互補(bǔ)動(dòng)物模型對(duì)這一過(guò)程進(jìn)行了研究。

他們發(fā)現(xiàn)，病原體向胎盤(pán)的轉(zhuǎn)移同時(shí)需要兩個(gè)毒性因子或入侵蛋白，即InlA 和 InlB。所以阻斷這兩個(gè)通道中的一個(gè)或?qū)⑵淙孔钄?，有可能阻止?xì)菌進(jìn)入胎兒體內(nèi)。反過(guò)來(lái)說(shuō),，人們也許有可能利用這兩個(gè)通道來(lái)輸送穿過(guò)同一障礙的治療用分子,。（生物谷Bioon.com）

生物谷推薦原始出處：

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.