Monoclonal antibodies responses against Enterotoxin of Clostridium perfringens using macro techniques culture

Abstract:
Clostridia pererfringens is anaerobic bacteria with sécrétion epsilon toxin that causes lethal enterotoxaemia in animals. In this study, cytotoxicity effects of two monoclonal neutralizing antibodies 4D7 and 5B7 were evaluated against epsilon toxin using an in vitro technique with staining MDCK cell culture. The effects of inhibitory of two monoclonal antibodies neutralize epsilon toxin of clostridia that were cultured on Madin Derby canine Kidney cells, MDCK cells by staining 7-actinodiamine dye. It was showed that the two neutralizing antibodies inhibited the pore forming activity of epsilon toxin and reduced the epsilon toxin bound to MDCK cells at 4oC. Epitopes, the two major 134, 145 amino acids were recognized by antibodies that neutralized the activities of epsilon toxin, By Competitive ELISA and microarray tests via that monoclonal antibody 4D7 were also diagnosed and analyzed134 and 145 epitopes It was shown that an amphipathic protein molecule was coated with toxin membrane. Therefore, this valuable information may be used in the development antitoxin therapies in the near future time.
Language:
Persian
Published:
Journal of Animan Researches, Volume:29 Issue: 1, 2016
Pages:
166 to 183
magiran.com/p1594607  
دانلود و مطالعه متن این مقاله با یکی از روشهای زیر امکان پذیر است:
اشتراک شخصی
با عضویت و پرداخت آنلاین حق اشتراک یک‌ساله به مبلغ 1,390,000ريال می‌توانید 70 عنوان مطلب دانلود کنید!
اشتراک سازمانی
به کتابخانه دانشگاه یا محل کار خود پیشنهاد کنید تا اشتراک سازمانی این پایگاه را برای دسترسی نامحدود همه کاربران به متن مطالب تهیه نمایند!
توجه!
  • حق عضویت دریافتی صرف حمایت از نشریات عضو و نگهداری، تکمیل و توسعه مگیران می‌شود.
  • پرداخت حق اشتراک و دانلود مقالات اجازه بازنشر آن در سایر رسانه‌های چاپی و دیجیتال را به کاربر نمی‌دهد.
In order to view content subscription is required

Personal subscription
Subscribe magiran.com for 70 € euros via PayPal and download 70 articles during a year.
Organization subscription
Please contact us to subscribe your university or library for unlimited access!