Gut Microbiota Imbalance: Can Light Therapy (PBMT) Help?

The critical role of the gut microbiome in human health is increasingly recognized, with imbalances (dysbiosis) linked to various diseases. This clinical research report explores photobiomodulation therapy (PBMT), a non-invasive approach using red and near-infrared light, as a potential modulator of gut microbiota. Emerging evidence suggests PBMT can beneficially influence gut microbiome composition, promoting beneficial bacteria, reducing inflammation, and affecting vitamin D levels. Supportive animal studies and theoretical frameworks indicate PBMT's promise in addressing gut-related disorders, including neurological conditions like Alzheimer's and Parkinson's. While highlighting PBMT's potential as an adjunctive therapy, this report underscores the need for further research to optimize its application.

The article explores the crucial role of the gut microbiome in health, highlighting the balance between beneficial and harmful bacteria. It defines dysbiosis as an imbalance linked to various diseases and introduces Photobiomodulation Therapy (PBMT), utilizing red (630–700 nm) and near-infrared (700–1200 nm) light, as a potential modulator of the gut microbiome, particularly for dysbiosis-related disorders.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10835098/#sec2

doi: 10.22037/ghfbb.v16i4.2687

The gut microbiota, containing approximately 10^14 bacterial cells (10 times more than human cells), significantly impacts health. Dysbiosis is associated with conditions like IBD and type 2 diabetes. Light, by influencing circadian rhythms, can affect the gut microbiota. PBMT has shown promise in stimulating healing and reducing inflammation. For example, Bicknell et al. found that PBMT (NIR 808 nm light, three times per week for 12 weeks) increased Allobaculum by 10,000-fold in healthy mice. Chen et al. showed that PBMT at 630 nm and 730 nm wavelengths decreased Helicobacter pylori and uncultured Bacteroidales, while increasing Rikenella in a mouse model of Alzheimer’s disease. Continuous light exposure increased Bacteroidales S24-7, while continuous dark exposure increased Bacteroidales and Rikenellaceae. A study showed a tenfold increase in epithelial commensal bacteria during the dark phase.

The gut microbiome, a focus of projects like the HMP and MetaHIT, consists of commensal and pathogenic microorganisms. Dysbiosis, an imbalance in the gut microbiome, leads to a decrease in beneficial bacteria and an increase in harmful ones. The dominant bacterial phyla are Firmicutes (approximately 64%) and Bacteroidetes (approximately 23%), making up about 90% of the gut microbiota. In a healthy state, the gut microbiome produces beneficial metabolites (SCFAs) with anti-inflammatory properties. SCFAs (acetate, propionate, and butyrate) regulate intestinal epithelial cell function and reduce inflammation. Conversely, Gram-negative bacterial lipopolysaccharides (LPS) induce pro-inflammatory cytokines (IL-6, MIP-3α, TNF-α), disrupting the gut barrier and leading to inflammation. The gut microbiome modulates macrophages, influencing inflammatory responses and maintaining intestinal homeostasis, which is crucial for preventing inflammatory diseases.

Dysbiosis plays a proven role in intestinal inflammation, linked to both Crohn's disease (CD) and ulcerative colitis (UC), which are types of IBD. Studies indicate that IBD patients show alterations in gut microbiota diversity and composition. Dysbiosis and changes in gut microbiota metabolites in IBD patients can lead to intestinal macrophage activation, an increased Th2/Th1 ratio, and stimulated IL-22 production, ultimately resulting in gut inflammation.

IBS is a gastrointestinal disorder with complex causes. Evidence suggests that dysbiosis triggers the activation of innate intestinal immune responses, increased expression of Toll-like receptors (e.g., TLR4) by macrophages, and enhanced production of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α). Additionally, in IBS patients, the adaptive immune response exhibits an imbalance in Th1/Th2 regulation and an increase in pro-inflammatory cytokines. Changes in gut microbiome composition observed in IBS patients include an increase in Lactobacillus, Veillonella, and Enterobacteriaceae, along with a decrease in Bifidobacterium and Clostridium compared to healthy individuals.

Celiac disease(CeD) is an autoimmune enteropathy triggered by immune reactions to undigested gliadin peptides. Dysbiosis contributes to CeD by disrupting the intestinal barrier, allowing gliadin peptides to cross into the lamina propria and provoke an immune response. Gram-negative bacteria (Bacteroidetes, Proteobacteria, Verrucomicrobia, and Fusobacteria) produce LPS, activating TLR4-associated inflammation and damaging the gut barrier. Conversely, Gram-positive bacteria like Lactobacilli and Bifidobacterium, considered probiotics, increase the expression of cell-binding protein to control inflammation. Studies indicate that Lactobacilli and Bifidobacterium species are decreased in CeD patients compared to controls.

Several hypotheses link the gut microbiome to brain function. Gut microbiota metabolomes (SCFAs, gamma-aminobutyric acid, noradrenaline, acetylcholine, dopamine, and serotonin) have neuroactive properties. The gut microbiome interacts with the central nervous system (CNS) via the gut-brain-microbiome axis. The microbiome produces LPS, a potential trigger for neuroinflammation that can contribute to neurological disorders. Studies indicate that patients with severe autism, amyotrophic lateral sclerosis, and Alzheimer's disease exhibit higher serum levels of this endotoxin compared to healthy individuals. Dysbiosis can overstimulate innate immune responses through Toll-like receptor 4 and activate oxidative stress, potentially triggering Parkinson's disease.

Photobiomodulation therapy was discovered by Endre Mester in 1967 (41). PBMT, or the use of red (630–700 nm) and near-infrared (700 and 1200 nm) light, has been shown to have the potential to be used as an adjunctive treatment option to reduce inflammation and accelerate pain and wound healing (42). In PBMT, photons penetrate the tissue and are absorbed by cytochrome c oxidase in mitochondria and calcium ion channels, which leads to increased enzyme activity, oxygen consumption, and ATP production (43). Furthermore, photons have the ability to dissociate nitric oxide (NO) into its active form from the heme and Cu centers of cytochrome c oxidase (44). Vasodilation and increased blood flow are two of the most important physiological processes in which NO is involved (45). In addition, under normal conditions, PBMT photons increase the production of reactive oxygen species (ROS), which leads to the activation of several transcription factors, increased gene expression, enhanced protein synthesis, etc. (7, 44). However, under conditions of oxidative stress and pathological states, PBMT decreases the production of ROS, NO, and NF-kB and induces anti-inflammatory effects (12). PMBT can reduce the production of prostaglandin E2 (PGE2) and pro-inflammatory cytokines such as IL-1ß, IL-6, IL-8, IL-12, and TNFα (32). Sousa et al. in 2017 showed that 660 nm PMB can significantly reduce the mRNA expression of TNFα, CCL,3, and CXCL2 by activating M1 macrophages 4 hours after irradiation (46). In another recent study, PBM was shown to modulate the ratio of M1 and M2 macrophage phenotypes, suppress a range of pro-inflammatory cytokines and chemokines associated with macrophages, and increase the concentration of anti-inflammatory cytokines in a time and wavelength-dependent manner (47).

The study produced the following results:

• Near-infrared light (808 nm): Increased allobaculum count 10,000-fold when applied to the abdomen.
• Light/dark exposure: Continuous dark exposure increased Bacteroidales and Rikenellaceae bacteria; continuous light exposure increased Bacteroidales S24-7 bacteria.
• Light stress: Caused a ten-fold increase in epithelial commensal bacteria during the dark phase.
• Sunlight/UVB: Seasonal variations altered microbiome composition. Reduced UVB exposure and vitamin D deficiency promoted gut dysbiosis.
• PBMT (630 nm and 730 nm): Decreased Helicobacter pylori and uncultured Bacteroidales, while increasing Rikenella. Improved Alzheimer's disease symptoms in a mouse model when applied to the head and abdomen.
• PBMT (head, nose, neck, abdomen): led to positive changes in the Firmicutes to Bacteroidetes ratio and improved clinical symptoms in Parkinson's disease.

PBMT is presented as a promising, non-invasive adjunctive therapy for conditions associated with gut microbiota. Further research is needed to determine optimal dosages and treatment regimens for specific conditions, but the therapy shows high tolerability and few side effects. PBMT can reduce a range of clinical symptoms of Parkinson's disease and affect the composition of the gut microbiome, showing positive changes in the Firmicutes to Bacteroidetes (F: B) ratio in these patients.

The information on this blog is for informational purposes only and does not constitute medical advice. Always consult a doctor or specialist before starting any therapy or treatment.