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A novel Shiga toxin 2a neutralizing antibody therapeutic with low immunogenicity and high efficacy.
Kirkland, Marina E; Patfield, Stephanie; Hughes, Anna C; Hernlem, Bradley; He, Xiaohua.
Afiliação
  • Kirkland ME; United States Department of Agriculture, Agricultural Research Service, Western Regional Research Center , Albany, California, USA.
  • Patfield S; U.S. Department of Energy, Oak Ridge Institute for Science and Education , Oak Ridge, Tennessee, USA.
  • Hughes AC; United States Department of Agriculture, Agricultural Research Service, Western Regional Research Center , Albany, California, USA.
  • Hernlem B; United States Department of Agriculture, Agricultural Research Service, Western Regional Research Center , Albany, California, USA.
  • He X; United States Department of Agriculture, Agricultural Research Service, Western Regional Research Center , Albany, California, USA.
Antimicrob Agents Chemother ; 68(1): e0059823, 2024 Jan 10.
Article em En | MEDLINE | ID: mdl-38047751
ABSTRACT
Shiga toxin-producing Escherichia coli infections are difficult to treat due to the risk of antibiotic-induced stress upregulating the production of toxins, medical treatment is consequently limited to supportive care to prevent the development of hemolytic uremic syndrome (HUS). Here, we introduce a potentially therapeutic humanized mouse monoclonal antibody (Hu-mAb 2-5) targeting Stx2a, the most common Shiga toxin subtype identified from outbreaks. We demonstrate that Hu-mAb 2-5 has low immunogenicity in healthy adults ex vivo and high neutralizing efficacy in vivo, protecting mice from mortality and HUS-related tissue damage.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Infecções por Escherichia coli / Escherichia coli Shiga Toxigênica / Síndrome Hemolítico-Urêmica Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Infecções por Escherichia coli / Escherichia coli Shiga Toxigênica / Síndrome Hemolítico-Urêmica Idioma: En Ano de publicação: 2024 Tipo de documento: Article