
Salmonella enterica Serovar Enteritidis tatB and tatC Mutants Are Impaired in Caco-2 Cell Invasion In Vitro and Show Reduced Systemic Spread in Chickens
Author(s) -
Claudia Mickael,
Po-King S. Lam,
Emil M. Berberov,
Brenda Allan,
Andrew Potter,
Wolfgang Köster
Publication year - 2010
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00090-10
Subject(s) - biology , salmonella enteritidis , microbiology and biotechnology , salmonella enterica , twin arginine translocation pathway , salmonella , mutant , biofilm , serotype , pathogen , virology , bacteria , gene , signal peptide , genetics , peptide sequence
Salmonella enterica subsp.enterica serovar Enteritidis is a leading causative agent of gastroenteritis in humans. This pathogen also colonizes the intestinal tracts of poultry and can spread systemically in chickens. Transfer to humans usually occurs through undercooked or improperly handled poultry meat or eggs. The bacterial twin-arginine transport (Tat) pathway is responsible for the translocation of folded proteins across the cytoplasmic membrane. In order to study the role of the Tat system in the infection and colonization of chickens bySalmonella Enteritidis, we constructed chromosomal deletion mutants of thetatB andtatC genes, which are essential components of the Tat translocon. We observed that thetat mutations affected bacterial cell morphology, motility, and sensitivity to albomycin, sodium dodecyl sulfate (SDS), and EDTA. In addition, the mutant strains showed reduced invasion of polarized Caco-2 cells. The wild-type phenotype was restored in all ourSalmonella Enteritidistat mutants by introducing episomal copies of thetatABC genes. When tested in chickens by use of aSalmonella Enteritidis ΔtatB strain, the Tat system inactivation did not substantially affect cecal colonization, but it delayed systemic infection. Taken together, our data demonstrated that the Tat system plays a role inSalmonella Enteritidis pathogenesis.