TLR4-mediated release of heparin-binding protein in human airways : a co-stimulatory role for IL-26
(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.
(Less)
- author
- Paulsson, Magnus LU ; Cardenas, Eduardo I ; Che, Karlhans F ; Brundin, Bettina ; Smith, Margaretha ; Qvarfordt, Ingemar and Lindén, Anders
- organization
- publishing date
- 2023
- 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}}, }