Differential effects of Th1, monocyte/macrophage and Th2 cytokine mixtures on early gene expression for molecules associated with metabolism, signaling and regulation in central nervous system mixed glial cell cultures

Lisak, Robert P.; Benjamins, Joyce A.; Bealmear, Beverly; Nedelkoska, Liljana; Studzinski, Diane; Retland, Ernest; Yao, Bin; Land, Susan

doi:10.1186/1742-2094-6-4

Cited by 38 publications

(33 citation statements)

References 221 publications

(212 reference statements)

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“…Changes in iNOS expression denote important pathological disturbances in oxidative stress-mediated damage in the human brain during HIV-1 infection 41,[55][56][57] and other neurodegenerative diseases. 58 Preferential increase in cerebellar Mac-1 expression in HIV-1 infected and CD8 ϩ cell depleted animals may be attributed to mouse brain anatomy and specificity of cell migration during inflammation.…”

Section: Discussionmentioning

confidence: 99%

Links between Progressive HIV-1 Infection of Humanized Mice and Viral Neuropathogenesis

Gorantla

Makarov

Finke-Dwyer

et al. 2010

The American Journal of Pathology

112

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Section: Discussionmentioning

confidence: 99%

Links between Progressive HIV-1 Infection of Humanized Mice and Viral Neuropathogenesis

Gorantla

Makarov

Finke-Dwyer

et al. 2010

The American Journal of Pathology

112

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“…Similar concentrations have been used in numerous in vitro studies, including ours [9][10][11]33], with effects on gene expression and cell function in many cell types. The physiologic relevance of the cytokine concentrations used in vitro can be debated.…”

Section: Protective Effects Of Cytokinesmentioning

confidence: 96%

“…The mixtures contained 10 ng/ml of each constituent cytokine as typically employed in a large number of in vitro systems, including our recent studies [9][10][11].…”

Section: Cytokine Mixturesmentioning

confidence: 99%

“…As one approach for identifying immunomodulatory mechanisms that affect oligodendroglia (OL) and white matter during ethanol exposure in early CNS development, we investigated the effects of ethanol on glial cultures, and asked whether proinflammatory or anti-inflammatory cytokines altered the glial responses. We used cytokine mixtures typical of those produced by Th1 or Th2 cells, or monocyte/macrophages (M/M) as used in our previous studies on effects of cytokines on gene expression in CNS glia [9][10][11]. In contrast to studies using a single cytokine and one glial population, we have examined the effects of these cytokine mixtures on glial cultures containing astroglia, microglia and OL to more closely model in vivo interactions.…”

Section: Introductionmentioning

confidence: 98%

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Cytokines Reduce Toxic Effects of Ethanol on Oligodendroglia

et al. 2011

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To characterize immunomodulatory mechanisms that affect oligodendroglia (OL) and white matter following ethanol exposure during early CNS development, we investigated the direct effects of ethanol and cytokines on glia. Mixed glial cultures from newborn rat brain were exposed to 6.5-130 mM ethanol for 1-3 days. OL were sensitive to ethanol, with death ranging from 32 to 88% with increasing time and ethanol concentrations. Little cell death occurred in astroglia or microglia. Mixtures of cytokines representative of those produced by pro-inflammatory Th1 and monocyte/macrophage (M/M) cells as well as those produced by anti-inflammatory Th2 cells were all protective. Three of the cytokines in the Th1 mixture, IL-2, TNF-α and IFN-γ, were protective individually, although no single cytokine was as effective as the mixture. The protective effects of the Th1 mixture and of IL-2 were reversed by inhibition of both MAP kinase and PI-3 kinase signaling pathways. We conclude that cytokines can act either directly on OL or indirectly through effects on astroglia or microglia to protect OL from ethanol toxicity.

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“…After the identifition of both T Cells and natural killer cells at the site of nerve injury in several rodent models, the involvement of T cells in NP was proposed 57 . Further, after transection of a spinal nerve , both cell types appear in the adjacent, uninjured DRG, although in lower numbers 58 .…”

Section: T-lymphocytesmentioning

confidence: 99%

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2012

IJPSR

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Neuropathic pain is considered as an inappropriate response caused by a lesion or dysfunction in the PNS or CNS). Neuropathic pain can manifest itself as either without a stimulus (stimulus-independent pain) and/ or as pain hypersensitivity elicited after a stimulus (stimulus-evoked pain). Stimulusindependent pain includes symptoms described by the patient such as (a) continuous, burning pain (b) intermittent shooting, lancinating pain (c) some dysaesthesias. Conversely, stimulus-evoked pain describes signs the physician induces after mechanical, thermal or chemical stimulation, and usually involves hyperalgesia or allodynia. The mechanism(s) underlying neuropathic pain are not completely understood but are considered to be complex, multifactorial and to evolve over time. Neuropathic pain can be trauma (surgical and non-surgical), accidents, and exposure to toxins, infection, viruses, metabolic diseases, nutritional deficiency, ischemia, and stroke. Current research studies indicate that both peripheral and central mechanisms have been involved in pathogenesis of neuropathic pain.

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Differential effects of Th1, monocyte/macrophage and Th2 cytokine mixtures on early gene expression for molecules associated with metabolism, signaling and regulation in central nervous system mixed glial cell cultures

Abstract: Background: Cytokines secreted by immune cells and activated glia play central roles in both the pathogenesis of and protection from damage to the central nervous system (CNS) in multiple sclerosis (MS).

Cited by 38 publications

References 221 publications

Links between Progressive HIV-1 Infection of Humanized Mice and Viral Neuropathogenesis

Links between Progressive HIV-1 Infection of Humanized Mice and Viral Neuropathogenesis

Cytokines Reduce Toxic Effects of Ethanol on Oligodendroglia

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