Chen Zhaochun, Moayeri Mahtab, Zhao Huaying, Crown Devorah, Leppla Stephen H, Purcell Robert H
Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Proc Natl Acad Sci U S A. 2009 Aug 11;106(32):13487-92. doi: 10.1073/pnas.0906581106. Epub 2009 Jul 27.
This study describes the isolation and characterization of a neutralizing monoclonal antibody (mAb) against anthrax edema factor, EF13D. EF13D neutralized edema toxin (ET)-mediated cyclic AMP (cAMP) responses in cells and protected mice from both ET-induced footpad edema and systemic ET-mediated lethality. The antibody epitope was mapped to domain IV of EF. The mAb was able to compete with calmodulin (CaM) for EF binding and displaced CaM from EF-CaM complexes. EF-mAb binding affinity (0.05-0.12 nM) was 50- to 130-fold higher than that reported for EF-CaM. This anti-EF neutralizing mAb could potentially be used alone or with an anti-PA mAb in the emergency prophylaxis and treatment of anthrax infection.
本研究描述了一种针对炭疽水肿因子EF13D的中和单克隆抗体(mAb)的分离与特性鉴定。EF13D可中和细胞中毒素(ET)介导的环磷酸腺苷(cAMP)反应,并保护小鼠免受ET诱导的足垫水肿以及全身性ET介导的致死作用。该抗体表位定位于EF的结构域IV。该mAb能够与钙调蛋白(CaM)竞争结合EF,并将CaM从EF-CaM复合物中置换出来。EF-mAb的结合亲和力(0.05-0.12 nM)比报道的EF-CaM的结合亲和力高50至130倍。这种抗EF中和mAb可能单独使用,或与抗PA mAb联合用于炭疽感染的紧急预防和治疗。