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Neutrophil-Derived Hyperresistinemia in Severe Acute Streptococcal Infections

Johansson, Linda; Linner, Anna; Sunden-Cullberg, Jonas; Haggar, Axana; Herwald, Heiko LU ; Lore, Karin; Treutiger, Carl-Johan and Norrby-Teglund, Anna (2009) In Journal of Immunology 183(6). p.4047-4054
Abstract
The concept of neutrophil activation and degranulation as important contributors to disease pathology in invasive group A streptococcal infections has recently been emphasized. This study focuses on two of the most severe streptococcal manifestations, toxic shock syndrome and necrotizing fasciitis, and the newly described proinflammatory molecule resistin, known to derive from adipocytes and monocytes. We demonstrate for the first time that these conditions are characterized by hyperresistinemia in circulation as well as at the local site of infection. Importantly, analyses of patient tissue biopsies and whole blood revealed that neutrophils represent a novel and dominant source of resistin in bacterial septic shock. This was confirmed by... (More)
The concept of neutrophil activation and degranulation as important contributors to disease pathology in invasive group A streptococcal infections has recently been emphasized. This study focuses on two of the most severe streptococcal manifestations, toxic shock syndrome and necrotizing fasciitis, and the newly described proinflammatory molecule resistin, known to derive from adipocytes and monocytes. We demonstrate for the first time that these conditions are characterized by hyperresistinemia in circulation as well as at the local site of infection. Importantly, analyses of patient tissue biopsies and whole blood revealed that neutrophils represent a novel and dominant source of resistin in bacterial septic shock. This was confirmed by the identification of resistin within neutrophil azurophilic granules. In vitro assays using primary neutrophils showed that resistin release was readily triggered by streptococcal cell wall components and by the streptococcal M1 protein, but not by the potent streptococcal superantigens. This is the first report demonstrating that resistin is released from neutrophils in response to microbial stimuli, which adds resistin to the neutrophil granule proteins that are likely to contribute to the pathologic inflammatory responses associated with severe streptococcal infections. The Journal of Immunology, 2009, 183: 4047-4054. (Less)
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author
organization
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type
Contribution to journal
publication status
published
subject
in
Journal of Immunology
volume
183
issue
6
pages
4047 - 4054
publisher
American Association of Immunologists
external identifiers
  • wos:000270179700059
  • scopus:70349320154
ISSN
1550-6606
DOI
10.4049/jimmunol.0901541
language
English
LU publication?
yes
id
e1b57540-445b-496a-a1c6-06cd3f27392b (old id 1490012)
date added to LUP
2009-10-21 10:29:30
date last changed
2017-07-02 04:02:26
@article{e1b57540-445b-496a-a1c6-06cd3f27392b,
  abstract     = {The concept of neutrophil activation and degranulation as important contributors to disease pathology in invasive group A streptococcal infections has recently been emphasized. This study focuses on two of the most severe streptococcal manifestations, toxic shock syndrome and necrotizing fasciitis, and the newly described proinflammatory molecule resistin, known to derive from adipocytes and monocytes. We demonstrate for the first time that these conditions are characterized by hyperresistinemia in circulation as well as at the local site of infection. Importantly, analyses of patient tissue biopsies and whole blood revealed that neutrophils represent a novel and dominant source of resistin in bacterial septic shock. This was confirmed by the identification of resistin within neutrophil azurophilic granules. In vitro assays using primary neutrophils showed that resistin release was readily triggered by streptococcal cell wall components and by the streptococcal M1 protein, but not by the potent streptococcal superantigens. This is the first report demonstrating that resistin is released from neutrophils in response to microbial stimuli, which adds resistin to the neutrophil granule proteins that are likely to contribute to the pathologic inflammatory responses associated with severe streptococcal infections. The Journal of Immunology, 2009, 183: 4047-4054.},
  author       = {Johansson, Linda and Linner, Anna and Sunden-Cullberg, Jonas and Haggar, Axana and Herwald, Heiko and Lore, Karin and Treutiger, Carl-Johan and Norrby-Teglund, Anna},
  issn         = {1550-6606},
  language     = {eng},
  number       = {6},
  pages        = {4047--4054},
  publisher    = {American Association of Immunologists},
  series       = {Journal of Immunology},
  title        = {Neutrophil-Derived Hyperresistinemia in Severe Acute Streptococcal Infections},
  url          = {http://dx.doi.org/10.4049/jimmunol.0901541},
  volume       = {183},
  year         = {2009},
}