Abstract
Porcine edema disease (ED) caused by Shiga toxin 2e producing Escherichia coli expressing F18ab+ fimbriae (F18ab+STEC) frequently occurs in post-weaned piglets, resulting in a significant economic loss in swine industries worldwide. In the present study, we proposed an efficient prevention scheme against ED in which the attenuated Salmonella Typhimurium inactivated by the E-mediated cell lysis to deliver target antigens, FedF and FedA, which function in fimbrial-mediated adhesion and as a major subunit of F18ab+fimbriae, respectively. The co-expression of FedA and FedF protein with outer membrane protein A signal peptide was confirmed in the resultant strains JOL1460 and JOL1464 by immunoblot analysis. Immunization with the candidate strains in mice led to the significant generation of immunoglobulin (Ig) G, specific to both antigens and secretory IgA specific to FedF (P < 0.05). The titers of IgG isotypes, IgG1 and IgG2a, used as markers for T-helpers (Th)-2 and Th-1lymphocytes, respectively, also significantly increased in the immunized group (P < 0.05). The increase in CD3+CD4+ T lymphocyte subpopulation and in vitro proliferative activity was observed in in vivo stimulated splenocytes, which indicated the immunostimulatory effect of the candidate strains. Moreover, the immunized mice were completely protected from a lethal challenge against wild-type F18+STEC whereas 28% of mice died in the non-immunized group. This study demonstrated that the inactivated Salmonella system could efficiently release FedF and FedA and induce robust immune responses specific to the target antigens, which is sufficient to protect the mice from the lethal challenge.
Highlights
Fimbrial adhesin F18 is frequently observed in enterotoxigenic Escherichia coli (ETEC) and Shiga toxin 2e producing E. coli (STEC) strains that cause diarrhea and edema disease (ED) in postweaned piglets, respectively, resulting in a significant burden on swine industries worldwide (Nagy et al, 1997)
The transmembrane tunnel generated on the surface of lysed JOL1460 and JOL1464 was identified by the scanning electron microscopy (SEM) techniques
The cell surface appeared to be partially collapsed by releasing cytoplasmic contents through the pores on the cell membrane (Figures 1B,C) compared to the morphology of normal cells (Figure 1A)
Summary
Fimbrial adhesin F18 is frequently observed in enterotoxigenic Escherichia coli (ETEC) and Shiga toxin 2e producing E. coli (STEC) strains that cause diarrhea and edema disease (ED) in postweaned piglets, respectively, resulting in a significant burden on swine industries worldwide (Nagy et al, 1997). Most F18ab+STEC isolates are associated with Shiga toxin 2e causing ED, while F18ac+ETEC produces enterotoxin ST-I. The STEC colonization in the small intestine is initiated by F18ab+ fimbriae-mediated adherence to the receptor on the brush border of the porcine enterocyte (Imberechts et al, 1992b). Shiga toxin released into the vascular endothelium induces inhibition of protein synthesis and cell death, causing submucosal edema and neurologic symptoms in weaned piglets (Imberechts et al, 1992a)
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