Journal
INFLAMMATION
Volume 44, Issue 4, Pages 1643-1661Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-021-01448-5
Keywords
COPD; bronchial epithelium; oxidative stress; IL-10; transcription factors; photobiomodulation
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Funding
- Foundation for Research Support of the State of Sao Paulo (FAPESP) [2012/16498-5]
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The study found that phototherapy has a dual effect on human bronchial epithelial cells activated by cigarette smoke extract. It downregulates the secretion of IL-8 and cAMP, while upregulating IL-10 through the Sp1 transcription factor.
The present study was aimed to investigate the phototherapy effect with lowlevel laser on human bronchial epithelial cells activated by cigarette smoke extract (CSE). Phototherapy has been reported to actuate positively for controlling the generation/release of anti-inflammatory and pro-inflammatory mediators from different cellular type activated by distinct stimuli. It is not known whether the IL-8 and IL-10 release from CSE-stimulated human bronchial epithelium (BEAS) cells can be influenced by phototherapy. Human bronchial epithelial cell (BEAS) line was cultured in a medium with CSE and irradiated (660 nm) at 9 J. Apoptosis index was standardized with Annexin V and the cellular viability was evaluated by MTT. IL-8, IL-10, cAMP, and NF-.B were measured by ELISA as well as the Sp1, JNK, ERK1/2, and p38MAPK. Phototherapy effect was studied in the presence of mithramycin or the inhibitors of JNK or ERK. The IL-8, cAMP, NF-.B, JNK, p38, and ERK1/2 were downregulated by phototherapy. Both the JNK and the ERK inhibitors potentiated the phototherapy effect on IL-8 as well as on cAMP secretion from BEAS. On the contrary, IL-10 and Sp1 were upregulated by phototherapy. The mithramycin blocked the phototherapy effect on IL-10. The results suggest that phototherapy has a dual effect on BEAS cells because it downregulates the IL-8 secretion by interfering with CSE-mediated signaling pathways, and oppositely upregulates the IL-10 secretion through of Sp1 transcription factor. Graphical Abstract
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