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TLR4-mediated release of heparin-binding protein in human airways : a co-stimulatory role for IL-26

Paulsson, Magnus LU orcid ; Cardenas, Eduardo I ; Che, Karlhans F ; Brundin, Bettina ; Smith, Margaretha ; Qvarfordt, Ingemar and Lindén, Anders (2023) In Frontiers in Immunology 14.
Abstract

BACKGROUND: Bacterial infection causes accumulation of neutrophils that release antimicrobial proteins including heparin-binding protein (HBP). In human airways, this neutrophil accumulation can be re-capitulated via intrabronchial exposure to lipopolysaccharide (LPS), a Toll-like receptor 4 (TLR4) agonist, that also causes a local increase in the neutrophil-mobilizing cytokine IL-26. Although LPS is considered a weak stimulus for HBP release
ex vivo, its effect on HBP release in human airways
in vivo has not been characterized.

METHODS: We determined whether intrabronchial exposure to LPS causes concomitant release of HBP and IL-26 in human airways, and whether IL-26 can enhance LPS-induced release of HBP in... (More)

BACKGROUND: Bacterial infection causes accumulation of neutrophils that release antimicrobial proteins including heparin-binding protein (HBP). In human airways, this neutrophil accumulation can be re-capitulated via intrabronchial exposure to lipopolysaccharide (LPS), a Toll-like receptor 4 (TLR4) agonist, that also causes a local increase in the neutrophil-mobilizing cytokine IL-26. Although LPS is considered a weak stimulus for HBP release
ex vivo, its effect on HBP release in human airways
in vivo has not been characterized.

METHODS: We determined whether intrabronchial exposure to LPS causes concomitant release of HBP and IL-26 in human airways, and whether IL-26 can enhance LPS-induced release of HBP in isolated human neutrophils.

RESULTS: We found that the concentration of HBP was markedly increased in bronchoalveolar lavage (BAL) fluid 12, 24, and 48 hours after LPS exposure, and that it displayed a strong and positive correlation with that of IL-26. Moreover, the concentration of HBP in conditioned media from isolated neutrophils was enhanced only after co-stimulation with LPS and IL-26.

CONCLUSIONS: Taken together, our findings indicate that TLR4 stimulation causes concomitant release of HBP and IL-26 in human airways, and that IL-26 may constitute a required co-stimulant for HBP release in neutrophils, thus enabling the concerted action of HBP and IL-26 in local host defense.

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author
; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Humans, Lipopolysaccharides/pharmacology, Toll-Like Receptor 4/metabolism, Carrier Proteins/metabolism, Blood Proteins/metabolism, Adjuvants, Immunologic
in
Frontiers in Immunology
volume
14
article number
1178135
publisher
Frontiers Media S. A.
external identifiers
  • scopus:85159943730
  • pmid:37234157
ISSN
1664-3224
DOI
10.3389/fimmu.2023.1178135
language
English
LU publication?
yes
id
b0e863d5-d8c5-4e34-8005-f037b6b9ec40
date added to LUP
2023-06-21 08:22:34
date last changed
2024-04-19 23:02:26
@article{b0e863d5-d8c5-4e34-8005-f037b6b9ec40,
  abstract     = {{<p>BACKGROUND: Bacterial infection causes accumulation of neutrophils that release antimicrobial proteins including heparin-binding protein (HBP). In human airways, this neutrophil accumulation can be re-capitulated via intrabronchial exposure to lipopolysaccharide (LPS), a Toll-like receptor 4 (TLR4) agonist, that also causes a local increase in the neutrophil-mobilizing cytokine IL-26. Although LPS is considered a weak stimulus for HBP release<br>
 ex vivo, its effect on HBP release in human airways <br>
 in vivo has not been characterized.<br>
 </p><p>METHODS: We determined whether intrabronchial exposure to LPS causes concomitant release of HBP and IL-26 in human airways, and whether IL-26 can enhance LPS-induced release of HBP in isolated human neutrophils.</p><p>RESULTS: We found that the concentration of HBP was markedly increased in bronchoalveolar lavage (BAL) fluid 12, 24, and 48 hours after LPS exposure, and that it displayed a strong and positive correlation with that of IL-26. Moreover, the concentration of HBP in conditioned media from isolated neutrophils was enhanced only after co-stimulation with LPS and IL-26.</p><p>CONCLUSIONS: Taken together, our findings indicate that TLR4 stimulation causes concomitant release of HBP and IL-26 in human airways, and that IL-26 may constitute a required co-stimulant for HBP release in neutrophils, thus enabling the concerted action of HBP and IL-26 in local host defense.</p>}},
  author       = {{Paulsson, Magnus and Cardenas, Eduardo I and Che, Karlhans F and Brundin, Bettina and Smith, Margaretha and Qvarfordt, Ingemar and Lindén, Anders}},
  issn         = {{1664-3224}},
  keywords     = {{Humans; Lipopolysaccharides/pharmacology; Toll-Like Receptor 4/metabolism; Carrier Proteins/metabolism; Blood Proteins/metabolism; Adjuvants, Immunologic}},
  language     = {{eng}},
  publisher    = {{Frontiers Media S. A.}},
  series       = {{Frontiers in Immunology}},
  title        = {{TLR4-mediated release of heparin-binding protein in human airways : a co-stimulatory role for IL-26}},
  url          = {{http://dx.doi.org/10.3389/fimmu.2023.1178135}},
  doi          = {{10.3389/fimmu.2023.1178135}},
  volume       = {{14}},
  year         = {{2023}},
}