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TLR4-mediated release of heparin-binding protein in human airways: a co-stimulatory role for IL-26
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)...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10206387/ https://www.ncbi.nlm.nih.gov/pubmed/37234157 http://dx.doi.org/10.3389/fimmu.2023.1178135 |
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author | Paulsson, Magnus Cardenas, Eduardo I. Che, Karlhans F. Brundin, Bettina Smith, Margaretha Qvarfordt, Ingemar Lindén, Anders |
author_facet | Paulsson, Magnus Cardenas, Eduardo I. Che, Karlhans F. Brundin, Bettina Smith, Margaretha Qvarfordt, Ingemar Lindén, Anders |
author_sort | Paulsson, Magnus |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-10206387 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-102063872023-05-25 TLR4-mediated release of heparin-binding protein in human airways: a co-stimulatory role for IL-26 Paulsson, Magnus Cardenas, Eduardo I. Che, Karlhans F. Brundin, Bettina Smith, Margaretha Qvarfordt, Ingemar Lindén, Anders Front Immunol Immunology 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. Frontiers Media S.A. 2023-05-10 /pmc/articles/PMC10206387/ /pubmed/37234157 http://dx.doi.org/10.3389/fimmu.2023.1178135 Text en Copyright © 2023 Paulsson, Cardenas, Che, Brundin, Smith, Qvarfordt and Lindén https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Paulsson, Magnus Cardenas, Eduardo I. Che, Karlhans F. Brundin, Bettina Smith, Margaretha Qvarfordt, Ingemar Lindén, Anders TLR4-mediated release of heparin-binding protein in human airways: a co-stimulatory role for IL-26 |
title | TLR4-mediated release of heparin-binding protein in human airways: a co-stimulatory role for IL-26 |
title_full | TLR4-mediated release of heparin-binding protein in human airways: a co-stimulatory role for IL-26 |
title_fullStr | TLR4-mediated release of heparin-binding protein in human airways: a co-stimulatory role for IL-26 |
title_full_unstemmed | TLR4-mediated release of heparin-binding protein in human airways: a co-stimulatory role for IL-26 |
title_short | TLR4-mediated release of heparin-binding protein in human airways: a co-stimulatory role for IL-26 |
title_sort | tlr4-mediated release of heparin-binding protein in human airways: a co-stimulatory role for il-26 |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10206387/ https://www.ncbi.nlm.nih.gov/pubmed/37234157 http://dx.doi.org/10.3389/fimmu.2023.1178135 |
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