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Secreted Group IIA Phospholipase A2 Protects Humans Against the Group B Streptococcus: Experimental and Clinical Evidence.

Movert, Elin LU ; Wu, Yongzheng ; Lambeau, Gérard ; Kahn, Fredrik LU ; Touqui, Lhousseine and Areschoug, Thomas LU (2013) In Journal of Infectious Diseases 208(12). p.2025-2035
Abstract
Group B streptococcus (GBS) is a leading neonatal pathogen and a growing cause of invasive disease in the elderly, with clinical manifestations such as pneumonia and sepsis. Despite its clinical importance, little is known about innate immunity against GBS in humans. Here, we analyze the role of human group IIA secreted phospholipase A2 (sPLA2-IIA), a bactericidal enzyme induced during acute inflammation, in innate immunity against GBS. We show that clinical GBS isolates are highly sensitive to killing by sPLA2-IIA but not by human antimicrobial peptides. Using transgenic mice that express human sPLA2-IIA, we demonstrate that this enzyme is crucial for host protection against systemic infection and lung challenge by GBS. We found that... (More)
Group B streptococcus (GBS) is a leading neonatal pathogen and a growing cause of invasive disease in the elderly, with clinical manifestations such as pneumonia and sepsis. Despite its clinical importance, little is known about innate immunity against GBS in humans. Here, we analyze the role of human group IIA secreted phospholipase A2 (sPLA2-IIA), a bactericidal enzyme induced during acute inflammation, in innate immunity against GBS. We show that clinical GBS isolates are highly sensitive to killing by sPLA2-IIA but not by human antimicrobial peptides. Using transgenic mice that express human sPLA2-IIA, we demonstrate that this enzyme is crucial for host protection against systemic infection and lung challenge by GBS. We found that acute sera from humans diagnosed with invasive GBS disease contain increased levels of sPLA2-IIA compared with normal sera from healthy individuals, indicating that GBS induces an sPLA2-IIA response in blood during human infection. We demonstrate that clinically relevant GBS strains are rapidly killed in these acute sera. We also demonstrate that the bactericidal effect is entirely due to sPLA2-IIA, showing that sPLA2-IIA might represent an important component of humoral innate immunity against GBS. Our data provide experimental and clinical evidence that sPLA2-IIA protects humans against GBS infections. (Less)
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author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Infectious Diseases
volume
208
issue
12
pages
2025 - 2035
publisher
Oxford University Press
external identifiers
  • wos:000327544600013
  • pmid:23901095
  • scopus:84897118527
  • pmid:23901095
ISSN
1537-6613
DOI
10.1093/infdis/jit359
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Division of Medical Microbiology (013250400), Division of Infection Medicine (SUS) (013008000)
id
c9d991ed-361b-4e01-bbaf-3f96f1fc5c2a (old id 4006392)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/23901095?dopt=Abstract
date added to LUP
2016-04-01 10:48:15
date last changed
2022-03-27 19:41:47
@article{c9d991ed-361b-4e01-bbaf-3f96f1fc5c2a,
  abstract     = {{Group B streptococcus (GBS) is a leading neonatal pathogen and a growing cause of invasive disease in the elderly, with clinical manifestations such as pneumonia and sepsis. Despite its clinical importance, little is known about innate immunity against GBS in humans. Here, we analyze the role of human group IIA secreted phospholipase A2 (sPLA2-IIA), a bactericidal enzyme induced during acute inflammation, in innate immunity against GBS. We show that clinical GBS isolates are highly sensitive to killing by sPLA2-IIA but not by human antimicrobial peptides. Using transgenic mice that express human sPLA2-IIA, we demonstrate that this enzyme is crucial for host protection against systemic infection and lung challenge by GBS. We found that acute sera from humans diagnosed with invasive GBS disease contain increased levels of sPLA2-IIA compared with normal sera from healthy individuals, indicating that GBS induces an sPLA2-IIA response in blood during human infection. We demonstrate that clinically relevant GBS strains are rapidly killed in these acute sera. We also demonstrate that the bactericidal effect is entirely due to sPLA2-IIA, showing that sPLA2-IIA might represent an important component of humoral innate immunity against GBS. Our data provide experimental and clinical evidence that sPLA2-IIA protects humans against GBS infections.}},
  author       = {{Movert, Elin and Wu, Yongzheng and Lambeau, Gérard and Kahn, Fredrik and Touqui, Lhousseine and Areschoug, Thomas}},
  issn         = {{1537-6613}},
  language     = {{eng}},
  number       = {{12}},
  pages        = {{2025--2035}},
  publisher    = {{Oxford University Press}},
  series       = {{Journal of Infectious Diseases}},
  title        = {{Secreted Group IIA Phospholipase A2 Protects Humans Against the Group B Streptococcus: Experimental and Clinical Evidence.}},
  url          = {{http://dx.doi.org/10.1093/infdis/jit359}},
  doi          = {{10.1093/infdis/jit359}},
  volume       = {{208}},
  year         = {{2013}},
}