Journal
BLOOD
Volume 116, Issue 13, Pages 2365-2372Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2010-02-271858
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Funding
- foundation of Ragnar and Torsten Soderberg
- foundation of Crafoord
- foundation of Greta and Johan Kock
- foundation of Alfred Osterlund
- foundation of Thelma Zoega
- Royal Physiographic Society in Lund
- Hansa Medical AB
- Swedish Research Council [7480, 12610, 21112]
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Streptococcus pyogenesis 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. (Blood. 2010;116(13):2365-2372)
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