Cytokines in Neuroinflammation and Alzheimers Disease

Cacquevel, Mathias; Lebeurrier, Nathalie; Chéenne, Simon; Vivien, Denis

doi:10.2174/1389450043345308

Cited by 219 publications

(144 citation statements)

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“…Because of the role of IL-6 in osteoclastogenesis (the formation of cells that function in the breakdown and resorption of bone tissue), an increased production of IL-6, as a consequence of the estrogen-depleted menopausal state, contributes to the increased resporption of bone which leads to osteoporosis . Recently, it has become clear that an overall increase in cytokine production, including TNFa, also increases the incidence of osteoporosis and other inflammatory conditions such as cardiovascular diseases and Alzheimer's disease (Pacifici, 1996;Ammann et al, 1997;Cacquevel et al, 2004). From in vitro studies it was found that estrogens can block DNA binding of NF-kB to kB site promoters (Stein and Yang, 1995;Galien and Garcia, 1997;An et al, 1999).…”

Section: Cross-talk Between Nf-jb and The Ermentioning

confidence: 99%

Cross-talk between nuclear receptors and nuclear factor κB

2006

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A variety of studies have shown that some activated nuclear receptors (NRs), especially the glucorticoid receptor, the estrogen receptor and peroxisome proliferator-activated receptor, can inhibit the activity of the transcription factor nuclear factor jB (NF-jB), which plays a key role in the control of genes involved in inflammation, cell proliferation and apoptosis. This review describes the molecular mechanisms of cross-talk between NRs and NF-jB and the biological relevance of this crosstalk. The importance and mechanistic aspects of selective NR modulation are discussed. Also included are future research prospects, which will lead to a new era in the field of NR research with the aim of specifically inhibiting NF-jB-driven gene expression for anti-inflammatory, anti-tumor and immune-modulatory purposes.

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Section: Cross-talk Between Nf-jb and The Ermentioning

confidence: 99%

Cross-talk between nuclear receptors and nuclear factor κB

2006

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“…Tumor necrosis factor (TNF)-α, a pleiotropic cytokine that exerts a variety of effects, such as growth promotion, growth inhibition, angiogenesis, cytotoxicity, inflammation, and immunomodulation [1], has been implicated in several inflammatory conditions [2][3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

Matera

Calzetta

Cazzola

2010

Pulmonary Pharmacology & Therapeutics

117

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Tumor necrosis factor (TNF)-α, a pleiotropic cytokine that exerts a variety of effects, such as growth promotion, growth inhibition, angiogenesis, cytotoxicity, inflammation, and immunomodulation, has been implicated in several inflammatory conditions. It plays a significant role in many inflammatory diseases of lung. Given that there is significant literature supporting the pathobiologic role of TNF-α in asthma, mainly in severe refractory asthma, and COPD, TNF-α inhibitors (infliximab, golimumab and etanercept) are now regarded as potential new medications in asthma and COPD management. The studies reported in literature indicate that TNF-α inhibitors are effective in a relatively small subgroup of patients with severe asthma, possibly defined by an increased TNF axis, but they seem to be ineffective in COPD, although an observational study demonstrated that TNF-α inhibitors were associated with a reduction in the rate of COPD hospitalisation among patients with COPD receiving these agents to treat their rheumatoid arthritis. These findings require a smart approach because there is still good reason to target TNF-α, perhaps in a more carefully selected patient group. TNF-α treatment should therefore not be thrown out, or abandoned. Indeed, since severe asthma and COPD are heterogeneous diseases that have characteristics that occur with different phenotypes remained poorly characterized and little known about the underlying pathobiology contributing to them, it is likely that definition of these phenotypes and choice of the right outcome measure will allow us to understand which kind of patients can benefit from TNF-α inhibitors.

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“…Interleukin 6 (IL-6) and interferon alpha (IFN-α) are two pro-inflammatory cytokines that play important roles during chronic inflammation (Sehgal 1990;Ershler 1993;Feghali and Wright 1997;Cacquevel et al 2004). Interestingly, IL-6 and IFN-α exert opposite effects on blood vessel formation; IL-6 is angiogenic (Campbell et al 1993), while IFN-α is angiostatic (Sidky and Borden 1987;Folkman and Ingber 1992).…”

Section: Introductionmentioning

confidence: 99%

Increased expression of the β4 and α5 integrin subunits in cerebral blood vessels of transgenic mice chronically producing the pro-inflammatory cytokines IL-6 or IFN-α in the central nervous system

Milner

Campbell

2006

Molecular and Cellular Neuroscience

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Evidence suggests that vascular function is strongly regulated by extracellular matrix (ECM) proteins via integrin-mediated signaling. To determine whether integrin expression on cerebral blood vessels is altered during chronic neuroinflammation, we examined β1 and β4 integrin expression in transgenic mice with astrocyte production of the pro-inflammatory cytokines interleukin-6 (IL-6) or interferon-α (IFN-α). Chronic production of IL-6 or IFN-α in the CNS promoted vascular expression of the β4 and α5 integrin subunits, and this was contributed mostly by astrocytes. Vascular expression of the ECM ligands laminin and fibronectin was also increased. Cell culture studies showed that astrocyte expression of the β4 and α5 integrins was significantly upregulated by IL-6 and IFN-α respectively, while endothelial expression of these integrins was unchanged. These results show that astrocytes respond to IL-6 and IFN-α by upregulating integrin expression. We propose that during neuroinflammation, astrocytes attempt to increase adhesive interactions at the blood-brain barrier (BBB), in order to increase barrier integrity.

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Cytokines in Neuroinflammation and Alzheimers Disease

Cited by 219 publications

References 0 publications

Cross-talk between nuclear receptors and nuclear factor κB

Cross-talk between nuclear receptors and nuclear factor κB

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

Increased expression of the β4 and α5 integrin subunits in cerebral blood vessels of transgenic mice chronically producing the pro-inflammatory cytokines IL-6 or IFN-α in the central nervous system

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