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Immune evasion by S...
Immune evasion by Staphylococcus aureus conferred by iron-regulated surface determinant protein IsdH.
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Visai, Livia (författare)
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Yanagisawa, Naoko (författare)
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- Josefsson, Elisabet, 1966 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning,Institute of Medicine, Department of Rheumatology and Inflammation Research
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visa fler...
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- Tarkowski, Andrej, 1951 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning,Institute of Medicine, Department of Rheumatology and Inflammation Research
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Pezzali, Ilaria (författare)
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Rooijakkers, Suzan H.M. (författare)
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Foster, Timothy J (författare)
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Speziale, Pietro (författare)
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visa färre...
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(creator_code:org_t)
- 2009
- 2009
- Engelska.
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Ingår i: Microbiology. - 1350-0872. ; 155:3, s. 667-679
- Relaterad länk:
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https://gup.ub.gu.se...
Abstract
Ämnesord
Stäng
- The ability of Staphylococcus aureus to avoid innate immune responses including neutrophil-mediated phagocytosis is crucial for the organism to cause infection. This multifactorial process involves several secreted and cell-surface-associated proteins. In this paper we report a novel mechanism of combating neutrophils that involves iron-regulated surface determinant protein H (IsdH). The IsdH protein is part of a complex that is only expressed under iron-restricted conditions in order to bind haemoglobin and extract and transport haem into the cytoplasm. A null mutant defective in expression of IsdH, and mutants expressing variants of IsdH with substitutions in residues predicted to be involved in ligand binding, were generated from S. aureus 8325-4. The IsdH-defective mutants were shown by several measures to have reduced virulence compared with the wild-type. The mutant was engulfed more rapidly by human neutrophils in the presence of serum opsonins, survived poorly in fresh whole human blood and was less virulent in a mouse model of sepsis. The protective mechanism seems to stem from an accelerated degradation of the serum opsonin C3b.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Mikrobiologi inom det medicinska området (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Microbiology in the medical area (hsv//eng)
Nyckelord
- Staphylococcus aureus
- adhesin
- sepsis
- virulens
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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