Lipopolysaccharide-binding protein increases toll-like receptor 4-dependent activation by nontypeable Haemophilus influenzae
Lazou Ahrén, Irini LU ; Bjartell, Anders LU ; Egesten, Arne LU and Riesbeck, Kristian LU
(2001)
In Journal of Infectious Diseases
184(7).
p.926-930
- Abstract
- Nontypeable Haemophilus influenzae (NTHi) is a common cause of respiratory tract infections. This study investigated the ability of NTHi to bind lipopolysaccharide-binding protein (LBP) derived from respiratory epithelial cells and the subsequent stimulation of transfected cells expressing membrane-bound CD14 and toll-like receptor 2 (TLR2) or TLR4. In the absence of LBP, NTHi at high concentrations (100 bacteria/epithelial cell) were required to induce signals through TLR2 and TLR4. Flow cytometry showed that NTHi in the stationary phase bound more LBP than did log-phase bacteria. Of interest, as few as 1 LBP-bearing bacterium/cell induced strong signaling through TLR4. In contrast, LBP bound to NTHi did not promote any increased... (More)
- Nontypeable Haemophilus influenzae (NTHi) is a common cause of respiratory tract infections. This study investigated the ability of NTHi to bind lipopolysaccharide-binding protein (LBP) derived from respiratory epithelial cells and the subsequent stimulation of transfected cells expressing membrane-bound CD14 and toll-like receptor 2 (TLR2) or TLR4. In the absence of LBP, NTHi at high concentrations (100 bacteria/epithelial cell) were required to induce signals through TLR2 and TLR4. Flow cytometry showed that NTHi in the stationary phase bound more LBP than did log-phase bacteria. Of interest, as few as 1 LBP-bearing bacterium/cell induced strong signaling through TLR4. In contrast, LBP bound to NTHi did not promote any increased signaling mediated by TLR2, compared with NTHi without LBP. These data suggest that, upon NTHi infection, low numbers of bacteria binding LBP may activate TLR4-bearing cells, such as alveolar macrophages, and consequently induce an inflammatory response. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1297208
- author
- Lazou Ahrén, Irini
LU
; Bjartell, Anders
LU
; Egesten, Arne
LU
and Riesbeck, Kristian
LU
- organization
- publishing date
- 2001
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Infectious Diseases
- volume
- 184
- issue
- 7
- pages
- 926 - 930
- publisher
- Oxford University Press
- external identifiers
-
- wos:000171228400018
- scopus:0035479059
- pmid:11528597
- ISSN
- 1537-6613
- DOI
- 10.1086/323398
- language
- English
- LU publication?
- yes
- id
- fb235e70-1300-4fce-8431-75be1428c6fd (old id 1297208)
- date added to LUP
- 2016-04-01 16:40:16
- date last changed
- 2022-04-22 23:39:43
@article{fb235e70-1300-4fce-8431-75be1428c6fd,
abstract = {{Nontypeable Haemophilus influenzae (NTHi) is a common cause of respiratory tract infections. This study investigated the ability of NTHi to bind lipopolysaccharide-binding protein (LBP) derived from respiratory epithelial cells and the subsequent stimulation of transfected cells expressing membrane-bound CD14 and toll-like receptor 2 (TLR2) or TLR4. In the absence of LBP, NTHi at high concentrations (100 bacteria/epithelial cell) were required to induce signals through TLR2 and TLR4. Flow cytometry showed that NTHi in the stationary phase bound more LBP than did log-phase bacteria. Of interest, as few as 1 LBP-bearing bacterium/cell induced strong signaling through TLR4. In contrast, LBP bound to NTHi did not promote any increased signaling mediated by TLR2, compared with NTHi without LBP. These data suggest that, upon NTHi infection, low numbers of bacteria binding LBP may activate TLR4-bearing cells, such as alveolar macrophages, and consequently induce an inflammatory response.}},
author = {{Lazou Ahrén, Irini and Bjartell, Anders and Egesten, Arne and Riesbeck, Kristian}},
issn = {{1537-6613}},
language = {{eng}},
number = {{7}},
pages = {{926--930}},
publisher = {{Oxford University Press}},
series = {{Journal of Infectious Diseases}},
title = {{Lipopolysaccharide-binding protein increases toll-like receptor 4-dependent activation by nontypeable Haemophilus influenzae}},
url = {{http://dx.doi.org/10.1086/323398}},
doi = {{10.1086/323398}},
volume = {{184}},
year = {{2001}},
}