Effect of photobiomodulation in an experimental in vitro model of asthma‐Copd overlap
The objective of the study was to evaluate the effect of photobiomodulation (PBM) with laser on the inflammatory process in an experimental in vitro model of ACO. The groups were: (1) human bronchial epithelial cells (BEAS‐2B); (2) BEAS‐2B cells treated with dexamethasone; (3) BEAS‐2B cells irradiat...
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Published in: | Journal of biophotonics Vol. 17; no. 10; pp. e202400124 - n/a |
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Main Authors: | , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Weinheim
WILEY‐VCH Verlag GmbH & Co. KGaA
01-10-2024
Wiley Subscription Services, Inc |
Subjects: | |
Online Access: | Get full text |
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Summary: | The objective of the study was to evaluate the effect of photobiomodulation (PBM) with laser on the inflammatory process in an experimental in vitro model of ACO. The groups were: (1) human bronchial epithelial cells (BEAS‐2B); (2) BEAS‐2B cells treated with dexamethasone; (3) BEAS‐2B cells irradiated with laser; (4) BEAS‐2B cells stimulated with cigarette smoke extract (CSE) + House Dust Mite (HDM); (5) BEAS‐2B cells stimulated with CSE + HDM and treated with dexamethasone; (6) BEAS‐2B cells incubated with CSE + HDM and irradiated with laser. After 24 h, cytokines were quantified. There was a reduction in TNF‐α, IL‐1β, IL‐6, IL‐4, IL‐5, IL‐13, IL‐17, IL‐21, IL‐23, and an increase in IL‐10 and IFN‐γ in cells from the laser‐irradiated ACO group compared to only ACO group. With these results, we can suggest that photobiomodulation acts in the modulation of inflammation observed in ACO, and may be a treatment option.
Human bronchial epithelial cells (BEAS‐2B) were stimulated with cigarette smoke extract (CSE) and house dust mite (HDM) for induction of the asthma‐COPD overlap (ACO). There was an increase in the secretion of inflammatory cytokines in the ACO group. Following photobiomodulation therapy (FBM), a reduction in inflammation was demonstrated with a decrease in the concentration of inflammatory cytokines and increase in IL‐10 and IFN‐γ. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1864-063X 1864-0648 1864-0648 |
DOI: | 10.1002/jbio.202400124 |