Phytotechnologies - Preventing Exposures, Improving Public Health

Phytotechnologies Have Potential to Reduce the Amount or Toxicity of Deleterious Chemicals and Agents, and Thereby, Can Reduce Human Exposures to Hazardous Substances. as Such, Phytotechnologies Are Tools for Primary Prevention in Public Health. Recent Research Demonstrates Phytotechnologies Can Be Uniquely Tailored for Effective Exposure Prevention in a Variety of Applications. in Addition to Exposure Prevention, Plants Can Be Used as Sensors to Identify Environmental Contamination and Potential Exposures. in This Paper, We Have Presented Applications and Research Developments in a Framework to Illustrate How Phytotechnologies Can Meet Basic Public Health Needs for Access to Clean Water, Air, and Food. Because Communities Can Often Integrate Plant-Based Technologies at Minimal Cost and with Low Infrastructure Needs, the Use of These Technologies Can Be Applied Broadly to Minimize Potential Contaminant Exposure and Improve Environmental Quality. These Natural Treatment Systems Also Provide Valuable Ecosystem Services to Communities and Society. in the Future, Integrating and Coordinating Phytotechnology Activities with Public Health Research Will Allow Technology Development Focused on Prevention of Environmental Exposures to Toxic Compounds. Hence, Phytotechnologies May Provide Sustainable Solutions to Environmental Exposure Challenges, Improving Public Health and Potentially Reducing the Burden of Disease. © 2013 Copyright Taylor and Francis Group, LLC

Microglia: neuroimmune-sensors of stress

Exposure to stressors disrupts homeostasis and results in the release of stress hormones including glucocorticoids, epinepherine and norepinepherine. Interestingly, stress also has profound affects on microglia, which are tissue-resident macrophages in the brain parenchyma. Microglia express a diverse array of receptors, which also allows them to respond to stress hormones derived from peripheral as well as central sources. Here, we review studies of how exposure to acute and chronic stressors alters the immunophenotype and function of microglia. Further, we examine a causal for stress hormones in these effects of stress on microglia. We propose that microglia serve as immunosensors of the stress response, which puts them in the unique position to sense and respond rapidly to alterations in homeostasis and integrate the neural response to threats.</p

Glucocorticoids mediate stress induction of the alarmin HMGB1 and reduction of the microglia checkpoint receptor CD200R1 in limbic brain structures

Exposure to stressors primes neuroinflammatory responses to subsequent immune challenges and stress-induced glucocorticoids (GCs) play a mediating role in this phenomenon of neuroinflammatory priming. Recent evidence also suggests that the alarmin high-mobility group&nbsp; box-1 (HMGB1) and the microglial checkpoint receptor CD200R1 serve as proximal mechanisms of stress-induced neuroinflammatory priming. However, it is unclear whether stress-induced GCs play a causal role in these proximal mechanisms of neuroinflammatory priming; this forms the focus of the present investigation. Here, we found that exposure to a severe acute stressor (inescapable tailshock) induced HMGB1 and reduced CD200R1 expression in limbic brain regions and pharmacological blockade of GC signaling (RU486) mitigated these effects of stress. To confirm these effects of RU486, adrenalectomy (ADX) with basal corticosterone (CORT) replacement was used to block the stress-induced increase in GCs as well as effects on HMGB1 and CD200R1. As with RU486, ADX mitigated the effects of stress on HMGB1 and CD200R1. Subsequently, exogenous CORT was administered to determine whether GCs are sufficient to recapitulate the effects of stress. Indeed, exogenous CORT induced expression of HMGB1 and reduced expression of CD200R1. In addition, exposure of primary microglia to CORT also recapitulated the effects of stress on CD200R1 suggesting that CORT acts directly on microglia to reduce expression of CD200R1. Taken together, these findings suggest that GCs mediate the effects of stress on these proximal mechanisms of neuroinflammatory priming.</p

Opioid-induced glial activation: mechanisms of activation and implications for opioid analgesia, dependence, and reward

© 2007 with author. Published by TheScientificWorldThis review will introduce the concept of toll-like receptor (TLR)-mediated glial activation as central to all of the following: neuropathic pain, compromised acute opioid analgesia, and unwanted opioid side effects (tolerance, dependence, and reward). Attenuation of glial activation has previously been demonstrated both to alleviate exaggerated pain states induced by experimental pain models and to reduce the development of opioid tolerance. Here we demonstrate that selective acute antagonism of TLR4 results in reversal of neuropathic pain as well as potentiation of opioid analgesia. Attenuating central nervous system glial activation was also found to reduce the development of opioid dependence, and opioid reward at a behavioral (conditioned place preference) and neurochemical (nucleus accumbens microdialysis of morphine-induced elevations in dopamine) level of analysis. Moreover, a novel antagonism of TLR4 by (+)- and (-)-isomer opioid antagonists has now been characterized, and both antiallodynic and morphine analgesia potentiating activity shown. Opioid agonists were found to also possess TLR4 agonistic activity, predictive of glial activation. Targeting glial activation is a novel and as yet clinically unexploited method for treatment of neuropathic pain. Moreover, these data indicate that attenuation of glial activation, by general or selective TLR antagonistic mechanisms, may also be a clinical method for separating the beneficial (analgesia) and unwanted (tolerance, dependence, and reward) actions of opioids, thereby improving the safety and efficacy of their use.Mark R. Hutchinson, Sondra T. Bland, Kirk W. Johnson, Kenner C. Rice, Steven F. Maier, and Linda R. Watkin