
Inactivation of the flagellin gene of Salmonella enterica serotype Enteritidis strongly reduces invasion into differentiated Caco‐2 cells
Author(s) -
Asten Fons J.A.M.,
Hendriks Henno G.C.J.M.,
Koninkx Jos F.J.G.,
Zeijst Bernard A.M.,
Gaastra Wim
Publication year - 2000
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2000.tb09058.x
Subject(s) - flagellin , complementation , salmonella enteritidis , mutant , salmonella enterica , biology , microbiology and biotechnology , serotype , gene , flagellum , enterobacteriaceae , shigella flexneri , salmonella , bacteria , escherichia coli , genetics
A nonflagellated mutant of Salmonella enterica serotype Enteritidis was constructed by disrupting the flagellin gene ( fliC ). Northern blot analysis indicated that the mutation did not affect expression of the downstream fliU gene. Infection experiments with differentiated Caco‐2 cells revealed that the mutant was about 50‐fold less invasive than the wild‐type strain, while bacterial adherence was unaffected. Complementation of the mutant with an intact fliC copy restored flagella formation and efficient bacterial invasion. Our data demonstrate that the fliC gene of S. enterica serotype Enteritidis is essential for the invasion of Caco‐2 cells.