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Microglial Cell Cultures (microglial + cell_culture)
Selected AbstractsMonocyte chemoattractant protein-1 (MCP-1) produced via NF-,B signaling pathway mediates migration of amoeboid microglia in the periventricular white matter in hypoxic neonatal ratsGLIA, Issue 6 2009Y. Y. Deng Abstract Monocyte chemoattractant protein-1 (MCP-1), a member of ,-chemokine subfamily, regulates the migration of microglia, monocytes, and lymphocytes to the inflammatory site in the central nervous system. We sought to determine if amoeboid microglial cells (AMC) produce MCP-1 that may be linked to migration of AMC in the corpus callosum periventricular white matter in hypoxic neonatal rats. A striking feature in 1-day-old rats subjected to hypoxia was a marked increase in cell numbers of AMC and immunoexpression of MCP-1 and its receptor (CCR2). By BrdU immunostaining, there was no significant change in the proliferation rate of AMC after hypoxic exposure when compared with the corresponding control rats. When injected intracerebrally into the corpus callosum of 7-day-old postnatal rats, MCP-1 induced the chemotactic migration of AMC to the injection site. In primary microglial cell culture subjected to hypoxia, there was a significant increase in MCP-1 release involving NF-,B signaling pathway. In in vitro chemotaxis assay, the medium derived from hypoxia-treated microglial cultures attracted more migratory microglial cells than that from the control microglial culture. The present results suggest that following a hypoxic insult, AMC in the neonatal rats increase MCP-1 production via NF-,B signaling pathway. This induces the migration and accumulation of AMC from the neighboring areas to the periventricular white matter (PWM). It is concluded that the preponderance and active migration of AMC, as well as them being the main cellular source of MCP-1, may offer an explanation for the PWM being susceptible to hypoxic damage in neonatal brain. © 2008 Wiley-Liss, Inc. [source] Expression of interleukin-1 receptors and their role in interleukin-1 actions in murine microglial cellsJOURNAL OF NEUROCHEMISTRY, Issue 4 2002Emmanuel Pinteaux Abstract Interleukin (IL)-1 is an important mediator of acute brain injury and inflammation, and has been implicated in chronic neurodegeneration. The main source of IL-1 in the CNS is microglial cells, which have also been suggested as targets for its action. However, no data exist demonstrating expression of IL-1 receptors [IL-1 type-I receptor (IL-1RI), IL-1 type-II receptor (IL-1RII) and IL-1 receptor accessory protein (IL-1RAcP)] on microglia. In the present study we investigated whether microglia express IL-1 receptors and whether they present target or modulatory properties for IL-1 actions. RT,PCR analysis demonstrated lower expression of IL-1RI and higher expression of IL-1RII mRNAs in mouse microglial cultures compared with mixed glial or pure astrocyte cultures. Bacterial lipopolysaccharide (LPS) caused increased expression of IL-1RI, IL-1RII and IL-1RAcP mRNAs, induced the release of IL-1,, IL-6 and prostaglandin-E2 (PGE2), and activated nuclear factor ,B (NF-,B) and the mitogen-activated protein kinases (MAPKs) p38, and extracellular signal-regulated protein kinase (ERK1/2), but not c-Jun N-terminal kinase (JNK) in microglial cultures. In comparison, IL-1, induced the release of PGE2, IL-6 and activated NF-,B, p38, JNK and ERK1/2 in mixed glial cultures, but failed to induce any of these responses in microglial cell cultures. IL-1, also failed to affect LPS-primed microglial cells. Interestingly, a neutralizing antibody to IL-1RII significantly increased the concentration of IL-1, in the medium of LPS-treated microglia and exacerbated the IL-1,-induced IL-6 release in mixed glia, providing the first evidence that microglial IL-1RII regulates IL-1, actions by binding excess levels of this cytokine during brain inflammation. [source] 1950,MHz IMT-2000 field does not activate microglial cells in vitroBIOELECTROMAGNETICS, Issue 2 2010Hideki Hirose Abstract Given the widespread use of the cellular phone today, investigation of potential biological effects of radiofrequency (RF) fields has become increasingly important. In particular, much research has been conducted on RF effects on brain function. To examine any biological effects on the central nervous system (CNS) induced by 1950,MHz modulation signals, which are controlled by the International Mobile Telecommunication-2000 (IMT-2000) cellular system, we investigated the effect of RF fields on microglial cells in the brain. We assessed functional changes in microglial cells by examining changes in immune reaction-related molecule expression and cytokine production after exposure to a 1950,MHz Wideband Code Division Multiple Access (W-CDMA) RF field, at specific absorption rates (SARs) of 0.2, 0.8, and 2.0,W/kg. Primary microglial cell cultures prepared from neonatal rats were subjected to an RF or sham field for 2,h. Assay samples obtained 24 and 72,h after exposure were processed in a blind manner. Results showed that the percentage of cells positive for major histocompatibility complex (MHC) class II, which is the most common marker for activated microglial cells, was similar between cells exposed to W-CDMA radiation and sham-exposed controls. No statistically significant differences were observed between any of the RF field exposure groups and the sham-exposed controls in percentage of MHC class II positive cells. Further, no remarkable differences in the production of tumor necrosis factor-, (TNF-,), interleukin-1, (IL-1,), and interleukin-6 (IL-6) were observed between the test groups exposed to W-CDMA signal and the sham-exposed negative controls. These findings suggest that exposure to RF fields up to 2,W/kg does not activate microglial cells in vitro. Bioelectromagnetics 31:104,112, 2010. © 2009 Wiley-Liss, Inc. [source] Nitric oxide and inflammationACTA OPHTHALMOLOGICA, Issue 2009AD DICK Purpose The talk will discuss the dichomatous role of nitric oxide in inflammation as a result of macrophage activation and also its role in controlling T cell responses. Methods We have used both microglial cell cultures, bone marrow derived macrophages and finally animal models of uveitis to dissect the role of macrophage activation and nitric oxide production in both tissue damage and limiting the extent of the inflammatory response. Results Macrophages when activated via T cell responses secreting interferon gamma, elicit a TNF-dependent nitrite response. Inhibiting nitric oxide activity by either suppressing NOS2 or via inhibiting TNF activity results in marked suppression of macrophage activation and reduction in retinal damage observed during experimental autoimmune uveoretinitis (EAU). Macrophages regulate T cell responses, in part via nitric oxide production, but is dependent upon IFN-gamma and autocrine TNF signalling via TNFReceptor1. Conclusion TNF and Interferon play essential roles in generating macrophage activation that elaborates in turn nitric oxide production. The nitric oxide, whilst damaging to cell membranes thus contributing to tissue damage during autoimmunity, also assists in regulating T cell responses by down regulating of T cell proliferation within the target tissue. [source] | ||||||||||