Microglia: Giving out dangerous signals - Cell Signaling Update - Signaling Gateway

"The release of heat-shock protein HSP60 from injured neurons activates Toll-like receptor 4 (TLR4) signaling, which stimulates microglia and facilitates neurodegeneration."

Read more: Microglia: Giving out dangerous signals - Cell Signaling Update - Signaling Gateway:

Neuroinflammation and Microglia: Considerations and approaches for neurotoxicity assessment

"Recent work, however, has clearly demonstrated that the cellular activities are, for the most part, beneficial. It is when the strict regulatory control normally imposed on them is altered that these cells may begin to show detrimental effects. One could speculate that such functions could be related to senescence and the inability to perform normal activities or the production of pro-inflammatory cytokines exceeding the down-regulatory capacity of the system with either an acute or chronic induction"

Harry, G. J. J. and Kraft, A. D. (2008). Neuroinflammation and microglia: considerations and approaches for neurotoxicity assessment. Expert opinion on drug metabolism & toxicology, 4(10):1265-1277. http://www.citeulike.org/user/HEIRS/article/7943439

Resveratrol differentially modulates inflam responses of microglia & astrocytes

Comment: An extremely useful read for those interested in this kind of stuff. Full text available.

"the first report of a difference between microglial cell and astrocyte in response to LPS, and of a difference in the capacity of resveratrol to protect microglia and astrocytes from inflammatory insults."


Lu, X., Ma, L., Ruan, L., Kong, Y., Mou, H., Zhang, Z., Wang, Z., Wang, J. M., and Le, Y. (2010). Resveratrol differentially modulates inflammatory responses of microglia and astrocytes. Journal of Neuroinflammation, 7(1):46+.  http://www.citeulike.org/user/HEIRS/article/7694580

Nair, S., Barve, A., Khor, T.-O. O., Shen, G.-X. X., Lin, W., Chan, J. Y., Cai, L., and Kong, A.-N. N. (2010). Regulation of nrf2- and ap-1-mediated gene expression by epigallocatechin-3-gallate and sulforaphane in prostate of nrf2-knockout or c57bl/6j mice and pc-3 ap-1 human prostate cancer cells. Acta pharmacologica Sinica. http://www.citeulike.org/user/HEIRS/article/7694509

Neuroprotective and Anti-inflammatory Activities of Ketogenic Diet on MPTP-induced Neurotoxicity.

Comments: I believe the results of this study are indicative of the fact that a keen understanding of the patients environmental illness and the factors that lead to it are crucial for the best holistic treatment and management of it. It is obvious that a one size fits treatment plan is probably not in the best interest of most patients.

"The change of dopamine was very similar to dopaminergic neurons in the SN. KD inhibited the activation of microglia induced by MPTP in the SN. The levels of proinflammatory cytokines (interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha) in the SN were also decreased and induced by MPTP. So, we concluded that KD was neuroprotective and anti-inflammatory against MPTP-neurotoxicity."

Read more: CiteULike: Neuroprotective and Anti-inflammatory Activities of Ketogenic Diet on MPTP-induced Neurotoxicity.:

DHA Suppresses Neuroinflammatory Responses and Induces Heme Oxygenase-1 Expression in BV-2 Microglia: Implications of Antidepressant Effects for Omega-3 Fatty Acids.

CiteULike: Docosahexaenoic Acid Suppresses Neuroinflammatory Responses and Induces Heme Oxygenase-1 Expression in BV-2 Microglia: Implications of Antidepressant Effects for Omega-3 Fatty Acids.: "Lu, D.-Y. Y., Tsao, Y.-Y. Y., Leung, Y.-M. M., and Su, K.-P. P. (2010). Docosahexaenoic acid suppresses neuroinflammatory responses and induces heme oxygenase-1 expression in bv-2 microglia: Implications of antidepressant effects for omega-3 fatty acids. Neuropsychopharmacology."

Release of Prostaglandin E2 and Nitric Oxide from Spinal Microglia Is Dependent on Activation of p38 Mitogen-Activated Protein Kinase.

TLR4: receptors that recognize liposaccharides on gram (-) bacteria that once activated trigger a number of different immune events.

"Our findings suggest that (a) activation of spinal microglia via TLR4 but not NK1 receptors produces PGE(2) and NO release from these cells; (b) the evoked PGE(2) release is generated by both COX-1 and COX-2, and (c) the COX-PGE(2) pathway is regulated by p38 and NOS2."

CiteULike: Release of Prostaglandin E2 and Nitric Oxide from Spinal Microglia Is Dependent on Activation of p38 Mitogen-Activated Protein Kinase.:

Mercury Induces Oxidative Stress, Altering Nrf2 Microglial~!

"Consistent with the nuclear translocation of Nrf2, quantitative real-time PCR revealed a concentration-dependent increase in the messenger RNA level of Ho-1, Nqo1, and xCT 30 min post MeHg exposure, whereas Nrf2 knockdown greatly reduced the upregulation of these genes. Furthermore, we observed increased microglial death upon Nrf2 knockdown by the small hairpin RNA approach. Taken together, our study has demonstrated that microglial cells are exquisitely sensitive to MeHg and respond rapidly to MeHg by upregulating the Nrf2-mediated antioxidant response."

CiteULike: Methylmercury Induces Acute Oxidative Stress, Altering Nrf2 Protein Level in Primary Microglial Cells:

Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2

In this study, we tested the hypothesis that HSV-induced neural cell oxidative tissue damage and cytotoxicity are mediated by microglial cell ROS through a TLR2-dependent mechanism. We detected elevated intracellular ROS in HSV-infected microglia obtained from wild-type mice. In contrast, the virus failed to induce ROS in microglia obtained from TLR2-/- mice. Additionally, compared to wild-type microglia, TLR2-/- microglia displayed attenuated HSV-induced lipid peroxidation and neurotoxicity. These studies demonstrate the importance of microglial cell TLR2 in inducing oxidative stress and neuronal damage in response to viral infection.

CiteULike: Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2: "Schachtele, S., Hu, S., Little, M., and Lokensgard, J. (2010). Herpes simplex virus induces neural oxidative damage via microglial cell toll-like receptor-2. Journal of Neuroinflammation, 7(1):35+."

Note: If high fat diets (HFD) influence the expression of TLR2 - one could assume that HFD may augment inflammatory responses. Diets that are lower in fat such as a typical Mediterranean Diet may reduce these inflammatory mediators and reduce symptoms. Other studies show that high glucose diets may also induce TLR expression (Dasu) and there is evidence that TR2 is necessary for development of the metabolic syndrome which makes one at higher risk for cardiovascular disease and diabetes (Himes).

For Further Reading: ImmunoGenetics in Autism, MCS and Cancer -- What Has Food Got To Do With It!

HEIRS Library Tags: TLR2


Dasu, M. R., Devaraj, S., Zhao, L., Hwang, D. H., and Jialal, I. (2008). High glucose induces toll-like receptor expression in human monocytes. Diabetes, 57(11):3090-3098.
http://www.citeulike.org/user/HEIRS/article/3207456
Himes, R. W. and Smith, C. W. (2009). Tlr2 is critical for diet-induced metabolic syndrome in a murine model. The FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
http://www.citeulike.org/user/HEIRS/article/6002948
Schachtele, S., Hu, S., Little, M., and Lokensgard, J. (2010). Herpes simplex virus induces neural oxidative damage via microglial cell toll-like receptor-2. Journal of Neuroinflammation, 7(1):35+.
http://www.citeulike.org/user/HEIRS/article/7366356
Lee, J. Y., Zhao, L., Youn, H. S., Weatherill, A. R., Tapping, R., Feng, L., Lee, W. H., Fitzgerald, K. A., and Hwang, D. H. (2004). Saturated fatty acid activates but polyunsaturated fatty acid inhibits toll-like receptor 2 dimerized with toll-like receptor 6 or 1. The Journal of biological chemistry, 279(17):16971-16979.
http://www.citeulike.org/user/HEIRS/article/3328606

Albumin activates astrocytes and microglia through mitogen-activated protein kinase pathways.

Albumin activates astrocytes and microglia through mitogen-activated protein kinase pathways.: "URL: Albumin activates astrocytes and microglia through mitogen-activated protein kinase pathways.

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Synergistic dopaminergic neurotoxicity of manganese and lipopolysaccharide: differential involvement of microglia and astroglia

Synergistic dopaminergic neurotoxicity of manganese and lipopolysaccharide: differential involvement of microglia and astroglia: "URL: Synergistic dopaminergic neurotoxicity of manganese and lipopolysaccharide: differential involvement of microglia and astroglia

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Sulforaphane suppresses lps-induced inflammation in primary rat microglia.

Notes: We showed that SF attenuates the LPS-induced increase of IL-1β, IL-6, and TNF-α expression in microglia. In addition, SF significantly decreases the NO in a concentration-dependent manner. SF inhibits LPS-stimulated ERK1/2 and JNK phosphorylation and thereby inhibits the LPS-induced activation of NF-κB- and activator protein-1 (AP-1). Moreover, SF and LPS together are able to induce Nrf2 activation.

Brandenburg, L.-O., Kipp, M., Lucius, R., Pufe, T., and Wruck, C. Sulforaphane suppresses lps-induced inflammation in primary rat microglia. Inflammation Research. http://www.citeulike.org/user/HEIRS/article/6195482

HEIRS LIbrary: Nrf2 regulates microglial dynamics and neuroinflammation in experimental Parkinson's disease

CiteULike: Nrf2 regulates microglial dynamics and neuroinflammation in experimental Parkinson's disease: "Rojo, A. I., Innamorato, N. G., Martín-Moreno, A. M., De Ceballos, M. L., Yamamoto, M., and Cuadrado, A. (2009). Nrf2 regulates microglial dynamics and neuroinflammation in experimental parkinson's disease. Glia, 9999(9999):NA+."

Manipulating brain inflammation may help clear brain of amyloid plaques, Mayo Clinic researchers say

"In a surprising reversal of long-standing scientific belief, researchers at the Mayo Clinic campus in Florida have discovered that inflammation in the brain is not the trigger that leads to buildup of amyloid deposits and development of Alzheimer's disease."


Manipulating brain inflammation may help clear brain of amyloid plaques, Mayo Clinic researchers say