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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1490012
- author
- Johansson, Linda
; Linner, Anna
; Sunden-Cullberg, Jonas
; Haggar, Axana
; Herwald, Heiko
LU
; Lore, Karin
; Treutiger, Carl-Johan
and Norrby-Teglund, Anna
- organization
- publishing date
- 2009
- 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
- pmid:19717514
- 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
- 2016-04-01 14:02:23
- date last changed
- 2022-04-22 01:00:33
@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}},
doi = {{10.4049/jimmunol.0901541}},
volume = {{183}},
year = {{2009}},
}