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Histidine-rich glycoprotein promotes bacterial entrapment in clots and decreases mortality in a mouse model of sepsis.

Abstract
Streptococcus pyogenes is a significant bacterial pathogen in humans. In this study, histidine-rich glycoprotein (HRG), an abundant plasma protein, was found to kill S pyogenes. Furthermore, S pyogenes grew more efficiently in HRG-deficient plasma, and clots formed in this plasma were significantly less effective at bacterial entrapment and killing. HRG-deficient mice were strikingly more susceptible to S pyogenes infection. These animals failed to control the infection at the local subcutaneous site, and abscess formation and inflammation were diminished compared with control animals. As a result, bacterial dissemination occurred more rapidly in HRG-deficient mice, and they died earlier and with a significantly higher mortality rate than control animals. HRG-deficient mice supplemented with purified HRG gave the same phenotype as control animals, demonstrating that the lack of HRG was responsible for the increased susceptibility. The results demonstrate a previously unappreciated role for HRG as a regulator of inflammation and in the defense at the local site of bacterial infection.
AuthorsOonagh Shannon, Victoria Rydengård, Artur Schmidtchen, Matthias Mörgelin, Per Alm, Ole E Sørensen, Lars Björck
JournalBlood (Blood) Vol. 116 Issue 13 Pg. 2365-72 (Sep 30 2010) ISSN: 1528-0020 [Electronic] United States
PMID20587784 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Blood Proteins
  • Proteins
  • histidine-rich proteins
Topics
  • Animals
  • Blood Coagulation (genetics, physiology)
  • Blood Proteins (deficiency, genetics, immunology, physiology)
  • Disease Models, Animal
  • Female
  • Humans
  • Immunity, Innate
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Microscopy, Electron, Transmission
  • Proteins (genetics, immunology, pharmacology, physiology)
  • Sepsis (blood, immunology, microbiology)
  • Streptococcal Infections (blood, immunology, microbiology)
  • Streptococcus pyogenes (growth & development, immunology, pathogenicity)

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