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Mostrando 13-24 de 40 artigos, teses e dissertações.
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13. Expression of Truncated Internalin A Is Involved in Impaired Internalization of Some Listeria monocytogenes Isolates Carried Asymptomatically by Humans
Fourteen human carriage Listeria monocytogenes isolates were compared to sporadic and epidemic-associated human strains in order to ascertain the pathogenic behavior of these unrecognized asymptomatic strains. Experimental infection of 14-day-old chick embryos revealed that the majority of the carriage strains were attenuated for virulence. Of the 10 attenua
American Society for Microbiology.
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14. Listeria monocytogenes σB Contributes to Invasion of Human Intestinal Epithelial Cells
The role of σB in Listeria monocytogenes infection of human intestinal epithelial cells was investigated. Invasion defects associated with loss of σB paralleled those of a ΔinlA strain independently of the σB-dependent P2prfA promoter. Concomitantly, amounts of inlA transcript and InlA protein were significantly decreased in the ΔsigB strain.
American Society for Microbiology.
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15. Truncated Internalin A and Asymptomatic Listeria monocytogenes Carriage: In Vivo Investigation by Allelic Exchange
Allelic exchange of the region coding for the C terminus of InlA between one epidemic (with an 80-kDa InlA) and one asymptomatic (with a 47-kDa InlA) carriage Listeria monocytogenes strain confirmed the need for this region for internalin entry in vitro. Interestingly, restoration of internalin A functionality did not result in full virulence in chicken embr
American Society for Microbiology.
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16. The inlA Gene of Listeria monocytogenes LO28 Harbors a Nonsense Mutation Resulting in Release of Internalin
Internalin is a surface protein that mediates entry of Listeria monocytogenes EGD into epithelial cells expressing the cell adhesion molecule human E-cadherin or its chicken homolog, L-CAM, which act as receptors for internalin. After observing that entry of L. monocytogenes LO28 into S180 fibroblasts, in contrast to that of EGD, did not increase after trans
American Society for Microbiology.
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17. Division of Listeria monocytogenes Serovar 1/2a Strains into Two Groups by PCR and Restriction Enzyme Analysis
Altogether, 100 strains of Listeria monocytogenes serovar 1/2a isolated from humans, animals, food, and the environment were typed by a combination of PCR and restriction enzyme analysis (REA). A PCR product of 2,916 bp, containing the downstream end of the gene inlA (955 bp), the space between inlA and inlB (85 bp), and 1,876 bp of the gene inlB, was cleave
American Society for Microbiology.
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18. Internalin of Listeria monocytogenes with an intact leucine-rich repeat region is sufficient to promote internalization.
Listeria monocytogenes can use two different surface proteins, internalin (InlA) and InlB, to invade mammalian cells. The exact role of these invasiveness factors in vivo remains to be determined. In cultured cells, InlA is necessary to promote Listeria entry into human epithelial cells, such as Caco-2 cells, whereas InlB is necessary to promote Listeria int
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19. Ribotypes and virulence gene polymorphisms suggest three distinct Listeria monocytogenes lineages with differences in pathogenic potential.
A total of 133 Listeria monocytogenes isolates were characterized by ribotyping and allelic analysis of the virulence genes hly, actA, and inlA to uncover linkages between independent phylogenetic and specific virulence markers. PCR-restriction fragment length polymorphisms revealed 8 hly, 11 inl4, and 2 actA alleles. The combination of these virulence gene
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20. Identification of four new members of the internalin multigene family of Listeria monocytogenes EGD.
Listeria monocytogenes is a bacterial pathogen that is able to invade nonphagocytic cells. Two surface proteins, internalin, the inlA gene product, and InlB, play important roles in the entry into cultured mammalian cells. These proteins also have extensive sequence similarities. Previously, Southern hybridization predicted the existence of an internalin mul
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21. Targeting and crossing of the human maternofetal barrier by Listeria monocytogenes: Role of internalin interaction with trophoblast E-cadherin
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. monocytogene
National Academy of Sciences.
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22. Identification and characterization of a novel PrfA-regulated gene in Listeria monocytogenes whose product, IrpA, is highly homologous to internalin proteins, which contain leucine-rich repeats.
The expression of all virulence factors in Listeria monocytogenes characterized to date is controlled by the virulence regulator protein, PrfA. To identify further PrfA-regulated proteins, we examined supernatants of L. monocytogenes EGD harboring additional copies of the PrfA regulator for the presence of novel proteins. This led to the identification and b
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23. Division of Listeria monocytogenes serovar 4b strains into two groups by PCR and restriction enzyme analysis.
Altogether, 133 strains of Listeria monocytogenes serovar 4b were investigated. A segment of 2,916 bp containing parts of the two genes inlA and inlB in L. monocytogenes was amplified by the PCR technique. The PCR product obtained was cleaved with the restriction enzyme AluI, and the fragments generated were separated by gel electrophoresis, leading to two d
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24. ClpC ATPase Is Required for Cell Adhesion and Invasion of Listeria monocytogenes
We studied the role of two members of the 100-kDa heat shock protein family, the ClpC and ClpE ATPases, in cell adhesion and invasion of the intracellular pathogen Listeria monocytogenes. During the early phase of infection, a clpC mutant failed to disseminate to hepatocytes in the livers of infected mice whereas the invasive capacity of a clpE mutant remain
American Society for Microbiology.