Stacy L Meyer’s research while affiliated with University of Wisconsin–Milwaukee and other places

What is this page?


This page lists works of an author who doesn't have a ResearchGate profile or hasn't added the works to their profile yet. It is automatically generated from public (personal) data to further our legitimate goal of comprehensive and accurate scientific recordkeeping. If you are this author and want this page removed, please let us know.

Publications (1)


Figure 1. 670 nm light modulates in vitro cytokine production by lymph node cells. Draining peripheral lymph nodes (PLN) were isolated at 10 days post immunization (dpi) from mice immunized with MOG 35-55. Single cell suspensions were cultured (A,B) in the presence or absence of MOG 35-55 or (C,D) with ConA (1 mg/mL) and were treated with 670 nm light (open symbols) or received no light treatment (closed symbols) once daily for 96 h. Cytokine ELISA was performed on supernatants for (A,C) IFN-c and (B,D) IL-10. Data reported as background-subtracted (e.g., in the absence of MOG 35-55 peptide) antigen-specific cytokine secretion. Data representative of 3 separate experiments. Error bars: SD. P,0.0001 by 2-way ANOVA. Multiple comparisons made via Bonferroni posttest; **P,0.01; ***P,0.001. doi:10.1371/journal.pone.0030655.g001
Figure 2. 670 nm light treatment reduces mean clinical score and signs of MOG-induced EAE. EAE was induced with MOG 35-55 , and mice were treated with 670 nm light or no light (restraint) stress [sham]. (A) Mice treated with the suppression protocol. 670 nm light (-%-; n = 8) or sham (-&-; n = 9). Representative 3 separate experiments with total n = 36 (670 nm light); n = 37 (sham). Error bars represent SEM. P,0.0001 by 2-way ANOVA. (B) Clinical course was plotted and the area under the curve (AUC) for all mice treated with the suppression protocol was determined and compared by 1-way ANOVA. Horizontal line: median value; Error bars: SEM. P,0.001. (C) duration of recovery for all mice treated with the suppression protocol was determined by counting the days of recovery from peak disease (decrease in 1 disease score) to the time of relapse (increase of 1 disease score); horizontal line: median value. (D) Mice were treated with 670 nm light (-%-; n = 10) or no light (restraint stress;-&-; n = 7) using the double-treatment protocol. Representative of 3 separate experiments with a total n = 24 (670 nm) or 2 separate experiments n = 14 (restraint only-sham). Error bars represent SEM. P,0.0001 by 2-way ANOVA. (E) The AUC of clinical disease curves for all mice treated with the double treatment was determined; horizontal line: median value. Error bars: SEM; P = 0.0003 by 1-Way ANOVA. **P,0.01; ***P,0.001. doi:10.1371/journal.pone.0030655.g002
Figure 3. The suppression treatment protocol results in cytokine modulation within the CNS over the course of EAE. Spinal cords (SC) were isolated from MOG 35-55-immunized mice treated with the suppression protocol and QPCR was performed to quantify cytokine gene expression. Relative gene expression was determined by the Paffl method (2000) Gene expression was normalized at each disease stage with sham treated mice. (A) INF-c; (B) TNF-a; (C) IL-4; (D) IL-10. n = 4 mice per group. Error bars indicated SD between 2 independent experiments. Data analyzed 2-way ANOVA. Multiple comparisons by Bonferroni post-test. *P,0.05, **P,0.01, ***P,0.0001, n.s = not significant. doi:10.1371/journal.pone.0030655.g003
Figure 4. The Double-Treatment protocol results in up-regulation of anti-inflammatory cytokines within the CNS over the course of EAE. Spinal cords (SC) were isolated from MOG 35-55-immunized mice treated with the double-treatment protocol and QPCR was performed to quantify cytokine gene expression. Gene expression was normalized at each disease stage with sham treated mice. (A) INF-c; (B) TNF-a; (C) IL-4; (D) IL-10. n = 4 mice per group. Error bars indicate SD between 2 independent experiments. Data were analyzed by 2-way ANOVA. Multiple comparisons by Bonferroni post-test. *P,0.05, **P,0.01, ***P,0.0001, n.s. = not significant. doi:10.1371/journal.pone.0030655.g004
Draining peripheral lymph nodes (PLN) were isolated at 10 days post immunization (dpi) from mice immunized with MOG35–55. Single cell suspensions were cultured (A,B) in the presence or absence of MOG35–55 or (C,D) with ConA (1 µg/mL) and were treated with 670 nm light (open symbols) or received no light treatment (closed symbols) once daily for 96 h. Cytokine ELISA was performed on supernatants for (A,C) IFN-γ and (B,D) IL-10. Data reported as background-subtracted (e.g., in the absence of MOG35–55 peptide) antigen-specific cytokine secretion. Data representative of 3 separate experiments. Error bars: SD. P<0.0001 by 2-way ANOVA. Multiple comparisons made via Bonferroni posttest; **P<0.01; ***P<0.001.

+3

Amelioration of Experimental Autoimmune Encephalomyelitis in C57BL/6 Mice by Photobiomodulation Induced by 670 nm Light
  • Article
  • Full-text available

January 2012

·

235 Reads

·

96 Citations

·

·

Stacy L Meyer

·

[...]

·

The approved immunomodulatory agents for the treatment of multiple sclerosis (MS) are only partially effective. It is thought that the combination of immunomodulatory and neuroprotective strategies is necessary to prevent or reverse disease progression. Irradiation with far red/near infrared light, termed photobiomodulation, is a therapeutic approach for inflammatory and neurodegenerative diseases. Data suggests that near-infrared light functions through neuroprotective and anti-inflammatory mechanisms. We sought to investigate the clinical effect of photobiomodulation in the Experimental Autoimmune Encephalomyelitis (EAE) model of multiple sclerosis. The clinical effect of photobiomodulation induced by 670 nm light was investigated in the C57BL/6 mouse model of EAE. Disease was induced with myelin oligodendrocyte glycoprotein (MOG) according to standard laboratory protocol. Mice received 670 nm light or no light treatment (sham) administered as suppression and treatment protocols. 670 nm light reduced disease severity with both protocols compared to sham treated mice. Disease amelioration was associated with down-regulation of proinflammatory cytokines (interferon-γ, tumor necrosis factor-α) and up-regulation of anti-inflammatory cytokines (IL-4, IL-10) in vitro and in vivo. These studies document the therapeutic potential of photobiomodulation with 670 nm light in the EAE model, in part through modulation of the immune response.

Download

Citations (1)


... Remote PBM may stimulate circulating immune cells, stem cells, mitochondria, and the cardiovascular and lymphatic systems. In an experimental autoimmune encephalomyelitis model, 670 nm remote PBM (5 J/cm 2 ) applied directly to the shaved dorsal surface of mice targeted the spinal cord, modulating immune responses and reducing central nervous system inflammation [162]. Another potential mechanism underlying remote PBM's effects may involve its impact on blood platelets, potentially increasing systemic ATP availability [163]. ...

Reference:

Photobiomodulation: shining a light on depression
Amelioration of Experimental Autoimmune Encephalomyelitis in C57BL/6 Mice by Photobiomodulation Induced by 670 nm Light