Shiga toxin 2e (Stx2e) has a pivotal role in the colonization and enterotoxicity of F18+Shiga toxin-producing Escherichia coli (STEC), which causes porcine edema disease (ED). In this study, a Stx2eA mutant, which has a Glu167Gln mutation in Stx2eA that inactivates N-glycosidase activity, was genetically engineered to evaluate its potential immunogenicity and protective efficacy. A significant increase in serum IgG1 (a Th2 indicator) was shown in mice immunized with the mutated Stx2eA. However, only 56% of the mice immunized with the toxoid (5 μg) survived following a challenge with a lethal dose 50 (LD50) of a virulent F18+STEC strain (JOL654), while mice immunized with Salmonella ghosts delivering selected antigens of F18+STEC showed an 86% survival rate. The results suggest that sole use of the mutated Stx2eA toxoid may not be an effective preventive strategy for the control of porcine ED.

Abstract
 서 론
 재료 및 방법
  동물 실험 윤리규정 Animals and ethics statement
  Stx2eA 톡소이드 발현 벡터의 구축 및 Stx2eA-His 발현대장균의 제작
  Stx2eA-His 발현 대장균주의 배양 및 Stx2eA-His의 정제
  체액성 면역 반응 및 도전 감염시 방어능 평가를 위한동물실험
  체내 독성 실험
  면역화된 마우스의 체액성 면역 반응
  통계분석
 결 과
  Stx2eA의 대장균 주에서 발현 여부 확인
  체내 독성 실험
  체액성 면역반응 유도 확인
  도전감염 시 방어능력 확인
 고 찰
 REFERENCES

• Gayeon Won(College of Veterinary Medicine, Chonbuk National University)
• Minsoo Choi(College of Veterinary Medicine, Chonbuk National University)
• John Hwa Lee(College of Veterinary Medicine, Chonbuk National University) Corresponding Author