Role of SefA subunit protein of SEF14 fimbriae in the pathogenesis of Salmonella enterica serovar Enteritidis.

Abstract

In this study, the role of the SefA subunit protein of SEF14 fimbriae in the pathogenesis of Salmonella enterica serovar Enteritidis was investigated. This was accomplished by mutating the sefA gene in the chromosome of two strains of S. enterica serovar Enteritidis by allelic exchange with a copy that has been inactivated by interruption with a nonpolar kanamycin resistance (aphA-3) cassette. The effect of this mutation on the ability of the S. enterica serovar Enteritidis strains to colonize the intestinal epithelium and to invade other tissues was assessed in BALB/c mice and in vitro by adherence and invasion of HeLa cells. Our results show that an avirulent S. enterica serovar Enteritidis vaccine strain, 11RX (no somatic antigen; flagellum antigen phase 1, g,m; flagellum antigen phase 2, -), colonized better and persisted longer in the Peyer's patches of these mice than did its SefA-deficient counterpart. However, no such difference was observed between a highly virulent S. enterica serovar Enteritidis strain, 7314 (somatic antigen, O1, O9, O12; flagellum antigen phase 1, g,m; flagellum antigen phase 2 [1,7]), and its SefA-deficient isogenic mutant. These findings were correlated with in vitro adherence and invasion of HeLa cells. Furthermore, we could not demonstrate a role for SefA in the virulence of S. enterica serovar Enteritidis as assessed by 50% lethal dose determinations. The implications of these findings are discussed.