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Evidence for antibody-catalyzed ozone formation in bacterial killing and inflammation

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Overview

related to degree

  • Takeuchi, Cindy, Ph.D. in Chemistry, Scripps Research 2000 - 2005
  • McDunn, Jonathan, Ph.D. in Biology, Scripps Research 1999 - 2003

authors

  • Wentworth Jr., Paul
  • McDunn, Jonathan
  • Wentworth, A. D.
  • Takeuchi, Cindy
  • Nieva, Jorge Javier
  • Jones, T.
  • Bautista, C.
  • Ruedi, J. M.
  • Gutierrez, A.
  • Janda, Kim
  • Babior, Bernard Macy
  • Eschenmoser, A.
  • Lerner, Richard

publication date

  • December 2002

journal

  • Science  Journal

abstract

  • Recently, we showed that antibodies catalyze the generation of hydrogen peroxide (H2O2) from singlet molecular oxygen (1O2*) and water. Here, we show that this process can lead to efficient killing of bacteria, regardless of the antigen specificity of the antibody. H2O2 production by antibodies alone was found to be not sufficient for bacterial killing. Our studies suggested that the antibody-catalyzed water-oxidation pathway produced an additional molecular species with a chemical signature similar to that of ozone. This species is also generated during the oxidative burst of activated human neutrophils and during inflammation. These observations suggest that alternative pathways may exist for biological killing of bacteria that are mediated by potent oxidants previously unknown to biology.

subject areas

  • Animals
  • Antibodies, Catalytic
  • Arthus Reaction
  • Blood Bactericidal Activity
  • Catalase
  • Catalysis
  • Escherichia coli
  • Hematoporphyrins
  • Humans
  • Hydrogen Peroxide
  • Indigo Carmine
  • Inflammation
  • Mice
  • Neutrophil Activation
  • Neutrophils
  • Oxidation-Reduction
  • Ozone
  • Rabbits
  • Rats
  • Rats, Sprague-Dawley
  • Respiratory Burst
  • Singlet Oxygen
  • Ultraviolet Rays
  • Water
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Identity

International Standard Serial Number (ISSN)

  • 0036-8075

Digital Object Identifier (DOI)

  • 10.1126/science.1077642

PubMed ID

  • 12434011
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Additional Document Info

start page

  • 2195

end page

  • 2199

volume

  • 298

issue

  • 5601

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