Article thumbnail
Location of Repository

Expression of Truncated Internalin A Is Involved in Impaired Internalization of Some Listeria monocytogenes Isolates Carried Asymptomatically by Humans

By Maïwenn Olier, Fabrice Pierre, Sandrine Rousseaux, Jean-Paul Lemaître, André Rousset, Pascal Piveteau and Jean Guzzo

Abstract

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 attenuated carriage strains, 5 were affected in their invasion capacities in vitro. Western blot analysis with antibody directed against InlA, the surface protein implicated in the internalization in host cells, allowed correlation between the ability of the carriage strains to enter Caco-2 cells and InlA expression. Indeed, these five carriage strains produced truncated forms of InlA. Four of the five truncated forms of InlA had an apparent molecular mass of 47 kDa. In order to assess the existence of a genetic lineage, partial sequences of inlA gene of these four strains were compared and revealed that they had a high degree of sequence conservation at the gene (99.86%) and amino acid (100%) levels. Comparison of their nucleotide sequences with that of the corresponding segment of inlA from EGD-e and Scott A strains, taken as epidemic references, showed more divergence. Taken together, these observations suggest the presence of specific traits that characterize L. monocytogenes strains isolated during asymptomatic carriage. Some of these traits could provide some explanations about the determinants that make them unable to cause systemic human infection

Topics: Cellular Microbiology: Pathogen-Host Cell Molecular Interactions
Publisher: American Society for Microbiology
Year: 2003
DOI identifier: 10.1128/IAI.71.3.1217-1224.2003
OAI identifier: oai:pubmedcentral.nih.gov:148840
Provided by: PubMed Central
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://dx.doi.org/10.1128/IAI.... (external link)
  • Suggested articles


    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.