Infrared light therapy relieves TLR-4 dependent hyper-inflammation of the type induced by COVID-19.
Blanche AguidaMarootpong PooamMargaret AhmadNathalie JourdanPublished in: Communicative & integrative biology (2021)
The leading cause of mortality from COVID-19 infection is respiratory distress due to an exaggerated host immune response, resulting in hyper-inflammation and ensuing cytokine storms in the lungs. Current drug-based therapies are of limited efficacy, costly, and have potential negative side effects. By contrast, photobiomodulation therapy, which involves periodic brief exposure to red or infrared light, is a noninvasive, safe, and affordable method that is currently being used to treat a wide range of diseases with underlying inflammatory conditions. Here, we show that exposure to two 10-min, high-intensity periods per day of infrared light causes a marked reduction in the TLR-4 dependent inflammatory response pathway, which has been implicated in the onset of cytokine storms in COVID-19 patients. Infrared light exposure resulted in a significant decline in NFkB and AP1 activity as measured by the reporter gene assay; decreased expression of inflammatory marker genes IL-6, IL-8, TNF-alpha, INF-alpha, and INF-beta as determined by qPCR gene expression assay; and an 80% decline in secreted cytokine IL6 as measured by ELISA assay in cultured human cells. All of these changes occurred after only 48 hours of treatment. We suggest that an underlying cellular mechanism involving modulation of ROS may downregulate the host immune response after Infrared Light exposure, leading to decrease in inflammation. We further discuss technical considerations involving light sources and exposure conditions to put these observations into potential clinical use to treat COVID-19 induced mortality.
Keyphrases
- immune response
- inflammatory response
- oxidative stress
- high intensity
- gene expression
- sars cov
- toll like receptor
- coronavirus disease
- high throughput
- poor prognosis
- dendritic cells
- lipopolysaccharide induced
- cell death
- dna methylation
- rheumatoid arthritis
- magnetic resonance
- stem cells
- risk assessment
- crispr cas
- transcription factor
- long non coding rna
- emergency department
- resistance training
- diabetic rats
- human health
- copy number
- replacement therapy
- single cell