Listeriosis in the Pregnant Guinea Pig: a Model of Vertical Transmission

Bakardjiev, Anna I.; Stacy, Brian A.; Fisher, Susan J.; Portnoy, Daniel A.

doi:10.1128/iai.72.1.489-497.2004

Cited by 126 publications

(111 citation statements)

References 60 publications

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“…As previously described, a limitation to the study of L. monocytogenes in vivo is that InlA and InlB interactions with their respective receptors are species-specific: InlA interacts with guinea pig E-cadherin, as in human, but not mouse and rat, E-cadherin (Lecuit et al 1999), whereas InlB interacts with mouse Met, as in human but not guinea pig Met (Khelef et al 2006). In apparent contradiction with the above epidemiological, ex vivo and in vitro results, InlA plays no role in L. monocytogenes fetoplacental infection in the guinea pig, despite its permissiveness to the InlA pathway (Bakardjiev et al 2004). Similarly, InlB plays no role in L. monocytogenes fetoplacental infection in the mouse, despite its permissiveness to the InlB pathway (Le Monnier et al 2007).…”

Section: Microbes and The Placental Barriermentioning

confidence: 69%

Concepts and Mechanisms: Crossing Host Barriers

Doran

Banerjee

Disson

et al. 2013

Cold Spring Harbor Perspectives in Medicine

111

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Section: Microbes and The Placental Barriermentioning

confidence: 69%

Concepts and Mechanisms: Crossing Host Barriers

Doran

Banerjee

Disson

et al. 2013

Cold Spring Harbor Perspectives in Medicine

111

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“…The recombinant sequence in pHK2 was used to replace the wild-type inlAB sequence in the chromosome of the L. monocytogenes 10403S strain by allelic exchange, as previously described (Camilli et al, 1993), to create strain FSL K4-009. DinlADsigB (strain FSL B2-042), DinlBDsigB (strain FSL K4-008), and DinlABDsigB (strain FSL K4-010) mutants were generated from strains DP-L4405 (Bakardjiev et al, 2004), HEL-137 (Kim et al, 2004) and FSL K4-009 (this study), respectively, by replacing the chromosomal allele of sigB with the DsigB allele of pTJA-57, as previously described (Wiedmann et al, 1998).…”

Section: Methodsmentioning

confidence: 99%

σ B contributes to Listeria monocytogenes invasion by controlling expression of inlA and inlB

2005

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The ability of Listeria monocytogenes to invade non-phagocytic cells is important for development of a systemic listeriosis infection. The authors previously reported that a L. monocytogenes DsigB strain is defective in invasion into human intestinal epithelial cells, in part, due to decreased expression of a major invasion gene, inlA. To characterize additional invasion mechanisms under the control of s B , mutants were generated carrying combinations of in-frame deletions in inlA, inlB and sigB. Quantitative assessment of bacterial invasion into the human enterocyte Caco-2 and hepatocyte HepG-2 cell lines demonstrated that s B contributes to both InlA and InlB-mediated invasion of L. monocytogenes. Previous identification of the s B -dependent P2 prfA promoter upstream of the major virulence gene regulator, positive regulatory factor A (PrfA), suggested that the contributions of s B to expression of various virulence genes, including inlA, could be at least partially mediated through PrfA. To test this hypothesis, relative invasion capabilities of DsigB and DprfA strains were compared. Exponential-phase cells of the DsigB and DprfA strains were similarly defective at invasion; however, stationary-phase DsigB cells were significantly less invasive than stationary-phase DprfA cells, suggesting that the contributions of s B to invasion extend beyond those mediated through PrfA in stationary-phase L. monocytogenes. TaqMan quantitative reverse-transcriptase PCRs further demonstrated that expression of inlA and inlB was greatly increased in a s B -dependent manner in stationary-phase L. monocytogenes. Together, results from this study provide strong biological evidence of a critical role for s B in L. monocytogenes invasion into non-phagocytic cells, primarily mediated through control of inlA and inlB expression.

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“…For example, in 178 cases of prenatal L. monocytogenes infection, 20% of pregnancies terminated in abortion or stillbirth, and 68% of live offspring were infected (9). This predisposition for fetal wastage and disseminated L. monocytogenes infection during pregnancy is not limited to only humans but widely reiterated across mammalian species, including nonhuman primates (10), ruminants (11,12), and rodents (13)(14)(15). Interestingly, our recent studies using mice bearing allogeneic pregnancies designed to recapitulate the natural heterogeneity between maternal MHC haplotype antigens and fetal MHC haplotype antigens indicate that prenatal L. monocytogenes infection-induced fetal resorption may not require direct in utero bacterial invasion (16).…”

Section: Introductionmentioning

confidence: 99%