Murine model of pregnancy-associated<i>Listeria monocytogenes</i>infection

Abram, Maja; Schlüter, Dirk; Vučković, Darinka; Wraber, Branka; Dorić, Miljenko; Deckert, Martina

doi:10.1016/s0928-8244(02)00449-2

Cited by 47 publications

(47 citation statements)

References 45 publications

(51 reference statements)

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“…Pregnant women constitute 60% of all cases of listeriosis in individuals Ͻ40 years of age (3). Their Ϸ20-fold higher risk of infection compared to otherwise healthy adults is presumed to be a consequence of the pregnancy-associated immunosuppression that allows tolerance of the fetoplacental allograft (4)(5)(6)(7). Nonetheless, the predilection of the fetoplacental unit for infection raises the possibility that a specific mechanism may be responsible for targeting L. monocytogenes to the maternofetal barrier.…”

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confidence: 99%

Targeting and crossing of the human maternofetal barrier byListeria monocytogenes: Role of internalin interaction with trophoblast E-cadherin

Lecuit

Nelson

Smith

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

209

177

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Listeria monocytogenes produces severe fetoplacental infections in humans. How it targets and crosses the maternofetal barrier is unknown. We used immunohistochemistry to examine the location of L. monocytogenes in placental and amniotic tissue samples obtained from women with fetoplacental listeriosis. The results raised the possibility that L. monocytogenes crosses the maternofetal barrier through the villous syncytiotrophoblast, with secondary infection occurring via the amniotic epithelium. Because epidemiological studies indicate that the bacterial surface protein, internalin (InlA), may play a role in human fetoplacental listeriosis, we investigated the cellular patterns of expression of its host receptor, E-cadherin, at the maternofetal interface. E-cadherin was found on the basal and apical plasma membranes of syncytiotrophoblasts and in villous cytotrophoblasts. Established trophoblastic cell lines, primary trophoblast cultures, and placental villous explants were each exposed to isogenic InlA؉ or InlA؊ strains of L. monocytogenes, and to L. innocua expressing or not InlA. Quantitative assays of cellular invasion demonstrated that bacterial entry into syncytiotrophoblasts occurs via the apical membrane in an InlA-E-cadherin dependent manner. In human placental villous explants, bacterial invasion of the syncytiotrophoblast barrier and underlying villous tissue and subsequent replication produces histopathological lesions that mimic those seen in placentas of women with listeriosis. Thus, the InlA-E-cadherin interaction that plays a key role in the crossing of the intestinal barrier in humans is also exploited by L. monocytogenes to target and cross the placental barrier. Such a ligand-receptor interaction allowing a pathogen to specifically cross the placental villous trophoblast barrier has not been reported previously.

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mentioning

confidence: 99%

Targeting and crossing of the human maternofetal barrier byListeria monocytogenes: Role of internalin interaction with trophoblast E-cadherin

Lecuit

Nelson

Smith

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

209

177

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“…Although feto-placental listeriosis has been induced in sheep (33) and recently in guinea pigs (6), most reports have used the murine model after intravenous inoculation. Under these conditions, feto-placental infection can be easily reproduced in pregnant mice (2,3,20,30,31,37). This experimental murine model presents several advantages for studying the pathogenesis of listeriosis, including the availability of many immunological and genetic tools.…”

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confidence: 99%

Invasion of the Placenta during Murine Listeriosis

et al. 2006

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Feto-placental infections due to Listeria monocytogenes represent a major threat during pregnancy, and the underlying mechanisms of placental invasion remain poorly understood. Here we used a murine model of listeriosis (pregnant mice, infected at day 14 of gestation) to investigate how this pathogen invades and grows within the placenta to ultimately infect the fetus. When L. monocytogenes is injected intravenously, the invasion of the placenta occurs early after the initial bacteremia, allowing the placental growth of the bacteria, which is an absolute requirement for vertical transmission to the fetus. Kinetically, bacteria first target the cells lining the central arterial canal of the placenta, which stain positively with cytokeratin, demonstrating their fetal trophoblast origin. Bacteria then disseminate rapidly to the other trophoblastic structures, like syncytiotrophoblast cells lining the villous core in the labyrinthine zone of placenta. Additionally, we found that an inflammatory reaction predominantly constituted of polymorphonuclear cells occurs in the villous placenta and participates in the control of infection. Altogether, our results suggest that the infection of murine placenta is dependent, at the early phase, on circulating bacteria and their interaction with endovascular trophoblastic cells. Subsequently, the bacteria spread to the other trophoblastic cells before crossing the placental barrier.

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“…monocytogenes infection elicits a comparable innate and acquired cellular immune response in humans and rodents; therefore, the murine model of L. monocytogenes infection has been widely used (1). Most previous mouse models used to assess strain invasiveness used intraperitoneal or intravenous inoculation of immunocompetent or immunocompromised mice (9,23,24,26).…”

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confidence: 99%

Oral Inoculation of A/J Mice for Detection of Invasiveness Differences between Listeria monocytogenes Epidemic and Environmental Strains

et al. 2004

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Four-week-old Harlan A/J mice were orally infected with six epidemic and six environmental strains of Listeria monocytogenes. Epidemic strains were significantly more invasive as a group than were environmental strains (P < 0.05), and the intestines of some mice infected with epidemic strains had extensive hemorrhage. Mice inoculated with epidemic strains were significantly more likely to become systemically infected than mice inoculated with environmental strains (P < 0.01).Listeria monocytogenes is a food-borne bacterial pathogen that can cause severe disease and high mortality in humans and animals (27). Although most epidemics are caused by L. monocytogenes serotype 4b, serotype 1/2a is the most common serotype isolated from food (4). This implies different virulence potential according to serotype. Other factors that may affect infectivity are the infective dose, survival of the bacteria in the gastrointestinal tract, and host immunity (15,27). Penetration of the intestinal barrier is the primary step for the infection (16), and subsequent invasion of organs such as the liver and spleen are also critical for establishing a systemic infection (27). Therefore, it is important to determine the ability of L. monocytogenes strains to penetrate the intestinal mucosa and invade organs by using an in vivo model to assess invasiveness.L. monocytogenes infection elicits a comparable innate and acquired cellular immune response in humans and rodents; therefore, the murine model of L. monocytogenes infection has been widely used (1). Most previous mouse models used to assess strain invasiveness used intraperitoneal or intravenous inoculation of immunocompetent or immunocompromised mice (9,23,24,26). However, most human infections are acquired orally, and these models do not address survival and translocation in the gut. Furthermore, studies describing intragastric infection of mice or guinea pigs required relatively high numbers of bacteria (10 9 CFU) (2,3,16,18,26). Recently, an A/J mouse model in which intragastric inoculation was used was described by Czuprynski et al. (6). It was found that 6-to 8-week-old A/J mice develop systemic infection following intragastric inoculation by using numbers of organisms similar to what is detected in L. monocytogenescontaminated food products. However, only two strains (Scott A and EGD) were tested (6), and sodium pentobarbital was used for anesthesia, which was later shown to increase susceptibility to infection (7). Therefore, it is important to test the efficacy of this model by using more strains and an alternative means of anesthesia.Mice. A previous study (22) tested NCR mice of various ages to assess the effect of mouse weight on the L. monocytogenes infection and demonstrated that smaller mice were more sensitive to oral infection and further suggested the use of 14-to 15-g mice (approximately 4 weeks old) for L. monocytogenes infection. Therefore, 4-week-old A/J mice (Harlan SpragueDawley, Indianapolis, Ind.) were used in this study (average weight, 14.1 Ϯ 1.6 g). Mice w...

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Murine model of pregnancy-associatedListeria monocytogenesinfection

Cited by 47 publications

References 45 publications

Targeting and crossing of the human maternofetal barrier byListeria monocytogenes: Role of internalin interaction with trophoblast E-cadherin

Targeting and crossing of the human maternofetal barrier byListeria monocytogenes: Role of internalin interaction with trophoblast E-cadherin

Invasion of the Placenta during Murine Listeriosis

Oral Inoculation of A/J Mice for Detection of Invasiveness Differences between Listeria monocytogenes Epidemic and Environmental Strains

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