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Effects of alpha 1-antitrypsin on endotoxin-induced lung inflammation in vivo

Subramaniyam, Devipriya; Steele, Chad; Koehnlein, Thomas; Welte, Tobias; Grip, Olof LU ; Matalon, Sadis and Janciauskiene, Sabina (2010) In Inflammation Research1995-01-01+01:00 59(7). p.571-578
Abstract
Previous in vitro experiments demonstrated that acute-phase protein, alpha 1-antitrypsin (AAT), could act either as an enhancer or as a suppressor of lipopolysaccharide (LPS)-induced cell activation depending on treatment time. Here we investigate how AAT regulates inflammatory responses in the short term when administrated post LPS challenge. Similar experimental setup was used both in vitro and in vivo: human monocytes and neutrophils were stimulated with LPS for 2 h followed by AAT for a total time of 4 h, and C57BL/6 mice were treated intranasally with LPS and 2 h later with AAT and sacrificed after 4 h. Bronchial lavage (BAL) and lung homogenates were analyzed using bio-plex cytokine assay. BAL cell counts were assessed. Within 4 h,... (More)
Previous in vitro experiments demonstrated that acute-phase protein, alpha 1-antitrypsin (AAT), could act either as an enhancer or as a suppressor of lipopolysaccharide (LPS)-induced cell activation depending on treatment time. Here we investigate how AAT regulates inflammatory responses in the short term when administrated post LPS challenge. Similar experimental setup was used both in vitro and in vivo: human monocytes and neutrophils were stimulated with LPS for 2 h followed by AAT for a total time of 4 h, and C57BL/6 mice were treated intranasally with LPS and 2 h later with AAT and sacrificed after 4 h. Bronchial lavage (BAL) and lung homogenates were analyzed using bio-plex cytokine assay. BAL cell counts were assessed. Within 4 h, AAT enhanced LPS-induced tumor necrosis factor-alpha (TNF alpha), interleukin (IL)-6, and IL-8 release from monocytes and neutrophils. Mice challenged for 4 h with LPS followed by AAT at 2 h showed no changes in BAL cell counts and higher levels of almost all measured cytokines, specifically RANTES in BAL and IL-12, IL-13, granulocyte colony-stimulating factor (G-CSF), granulocyte macrophage colony-stimulating factor (GM-CSF), and IL-10 levels in lung homogenates, than in mice treated with LPS only. Within the short term, AAT enhances the magnitude of LPS-induced specific cytokine/chemokine production, which may play an important role in amplification and resolution of acute-phase inflammatory reactions in vivo. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Inflammation, Cytokines, Alpha 1-antitrypsin, Endotoxin, Acute-phase proteins
in
Inflammation Research1995-01-01+01:00
volume
59
issue
7
pages
571 - 578
publisher
Birkhaüser
external identifiers
  • wos:000278579000010
  • scopus:77955702672
ISSN
1420-908X
DOI
10.1007/s00011-010-0164-x
language
English
LU publication?
yes
id
16036f8e-d937-4adf-bd36-e61702b8255a (old id 1631034)
date added to LUP
2010-07-21 14:16:47
date last changed
2018-05-29 10:02:20
@article{16036f8e-d937-4adf-bd36-e61702b8255a,
  abstract     = {Previous in vitro experiments demonstrated that acute-phase protein, alpha 1-antitrypsin (AAT), could act either as an enhancer or as a suppressor of lipopolysaccharide (LPS)-induced cell activation depending on treatment time. Here we investigate how AAT regulates inflammatory responses in the short term when administrated post LPS challenge. Similar experimental setup was used both in vitro and in vivo: human monocytes and neutrophils were stimulated with LPS for 2 h followed by AAT for a total time of 4 h, and C57BL/6 mice were treated intranasally with LPS and 2 h later with AAT and sacrificed after 4 h. Bronchial lavage (BAL) and lung homogenates were analyzed using bio-plex cytokine assay. BAL cell counts were assessed. Within 4 h, AAT enhanced LPS-induced tumor necrosis factor-alpha (TNF alpha), interleukin (IL)-6, and IL-8 release from monocytes and neutrophils. Mice challenged for 4 h with LPS followed by AAT at 2 h showed no changes in BAL cell counts and higher levels of almost all measured cytokines, specifically RANTES in BAL and IL-12, IL-13, granulocyte colony-stimulating factor (G-CSF), granulocyte macrophage colony-stimulating factor (GM-CSF), and IL-10 levels in lung homogenates, than in mice treated with LPS only. Within the short term, AAT enhances the magnitude of LPS-induced specific cytokine/chemokine production, which may play an important role in amplification and resolution of acute-phase inflammatory reactions in vivo.},
  author       = {Subramaniyam, Devipriya and Steele, Chad and Koehnlein, Thomas and Welte, Tobias and Grip, Olof and Matalon, Sadis and Janciauskiene, Sabina},
  issn         = {1420-908X},
  keyword      = {Inflammation,Cytokines,Alpha 1-antitrypsin,Endotoxin,Acute-phase proteins},
  language     = {eng},
  number       = {7},
  pages        = {571--578},
  publisher    = {Birkhaüser},
  series       = {Inflammation Research1995-01-01+01:00},
  title        = {Effects of alpha 1-antitrypsin on endotoxin-induced lung inflammation in vivo},
  url          = {http://dx.doi.org/10.1007/s00011-010-0164-x},
  volume       = {59},
  year         = {2010},
}