S100b expression in and effects on microglia

Adami, Cecilia; Sorci, Guglielmo; Blasi, Elisabetta; Agneletti, Anna Lisa; Bistoni, Francesco; Donato, Rosario

doi:10.1002/1098-1136(200102)33:2<131::aid-glia1012>3.0.co;2-d

Cited by 186 publications

(121 citation statements)

References 66 publications

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“…Although the studies mentioned above favor S100B as a contributing factor to amyloid deposition, contrastingly some animal studies have shown that the chronic elevation of S100B was not necessarily associated with increased expression of b-amyloid precursor protein mRNA and increased amyloid deposition (Reeves et al 1994;Yao et al 1995). S100B has also been shown to interact with the cerebral immune system like causing the secretion of pro-inflammatory cytokines and stimulating NO secretion which are involved in neurodegeneration and neuroinflammation (Hu et al 1996;Li et al 2000;Adami et al 2001). Glial cells are transiently activated by stress which is a normal physiological response.…”

Section: Discussionmentioning

confidence: 99%

Elevated S100B and Neuron Specific Enolase Levels in Patients with Migraine-without Aura: Evidence for Neurodegeneration?

et al. 2011

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Although migraine has mainly been considered as a benign disease, there is cumulative evidence of silent changes in the brain, brainstem, or cerebellum and subtle subclinical cerebellar dysfunction. In this study, in order to investigate a possible neuronal and/or glial damage at the cellular level in migraine, we measured and compared serum levels of S100B which is a protein marker of glial damage or activation, and neuron specific enolase (NSE) which is a marker of neuronal damage, in migraine patients and control subjects. Serum levels of S100B and NSE were measured in blood samples from 41 patients with migraine-without aura taken during a migraine attack (ictal) and in the attack-free period between migraine attacks (interictal) and 35 age- and sex-matched controls. Patients with migraine-without aura had significantly higher ictal serum levels of S100B and NSE (P < 0.05, for both) than control subjects; whereas in the interictal phase, there was a significant increment only in S100B levels (P < 0.05) compared to controls. On the other hand, serum levels of S100B and NSE in ictal and interictal blood samples did not differ significantly. The findings of increased ictal serum S100B and NSE levels together with increased interictal levels of S100B suggested that migraine might be associated with glial and/or neuronal damage in the brain and a prolonged disruption of blood-brain barrier. Increased interictal serum levels of S100B might point out to an insidious and slow damaging process in migraine patients.

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Section: Discussionmentioning

confidence: 99%

Elevated S100B and Neuron Specific Enolase Levels in Patients with Migraine-without Aura: Evidence for Neurodegeneration?

et al. 2011

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“…This result was somehow expected, since it is known [6] that macrophage secretory response to fungi may occur without ingestion, thus implying that Nramp1-expressing intracellular compartment(s) is not involved. Finally, it is worth noting that, although immortalized via an oncogene carrying retrovirus [27,38], the cell lines used in these studies consistently retain the phenotype of the primary macrophage cultures both at the functional and molecular level [1,3,6,7,26,27,38], thus arguing on the accuracy and usefulness of the continuous cell line model employed.…”

Section: Discussionmentioning

confidence: 89%

“…The cell lines had been obtained by immortalization of primary cultures via introducing retroviral oncogenes. They expressed and retained the phenotypical peculiarities of the original cultures and have been extensively used for functional and molecular studies on macrophages [1,3,6,7,26,27,38].…”

Section: Cell Linesmentioning

confidence: 99%

Nramp1 gene affects selective early steps in macrophage-mediated anti-cryptococcal defense

Blasi

Colombari

Mucci

et al. 2001

Med Microbiol Immunol

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Cryptococcus neoformans is an opportunistic fungus responsible for severe and often recurrent meningoencephalitis in immunodepressed patients. Initial evidence suggests that C. neoformans is a facultative intracellular pathogen; however, the strategies by which C. neoformans undergoes survival and eventually proliferation have not been elucidated. We investigated the role of Nrampl gene in macrophage-mediated anti-cryptococcal defense. Using cell lines expressing the functional, mutated or knockout gene, it was established that Nramp1 (1) is not involved in the phagocytic event, (2) influences anti-cryptococcal activity in the early steps but not at later times, and (3) is unrelated to the biomolecular pathways through which C. neoformans impairs macrophage secretory response. Although the functional role of Nramp1 is still far from being elucidated, the present data add insight into its involvement in macrophage-mediated antimicrobial defense, particularly in the initial steps allowing C. neoformans growth inhibition.

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“…4C, unlike mock controls, RR4 cells exposed to TCA produced significant and time-dependent amounts of NO. LPS-treated cells showed the expected (Adami et al, 2001;Stuehr et al, 1989;Puliti et al, 1999) NO production. ANOVA analysis showed significant differences among all groups at any time point (p = 0.000).…”

Section: Cytokines and No Productionmentioning

confidence: 79%

A Transmissible Cytotoxic Activity Isolated from a Patient with Brain Ischemia Causes Microglial Cell Activation and Dysfunction

et al. 2007

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1. Microglial cell activation occurs during brain injury, ischemia, and in several neurologic disorders. Recently, we isolated a transmissible cytotoxic activity (TCA) from the cerebrospinal fluid of a patient with brain ischemia. Such a TCA, associated with one or more protein(s) that supposedly had undergone in vivo misfolding, causes apoptosis in vitro in different cell lines, including microglial cells. The TCA producing cells and the potential in vivo role of such cytotoxic activity remains to be elucidated. Here, we investigated the in vitro effects of TCA on microglial cell immune functions.2. The murine microglial cell line RR4 was exposed to TCA, and then its response was evaluated as: (a) phagocytosis and antifungal activity against Candida albicans; (b) secretory pattern; and (c) levels of p38 phosphorylation.3. Unlike mock-treated controls, microglial cells exposed to TCA showed an increase in phagocytic activity. Unexpectedly, their capability to kill the ingested fungi significantly diminished. Moreover, TCA-treated cells produced amounts of macrophage inflammatory protein 1-alpha, tumor necrosis factor-alpha, and nitric oxide significantly higher than mock-treated cells. Finally, phosphorylation of p38 mitogen-activated protein kinase (MAPK) was detected in TCA-treated but not in mock-treated controls as early as 30 min after treatment.4. Overall, these results indicate that TCA causes a rapid molecular response in microglial cells, by the time, leading to an intriguing effector and secretory dysfunction.

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S100b expression in and effects on microglia

Cited by 186 publications

References 66 publications

Elevated S100B and Neuron Specific Enolase Levels in Patients with Migraine-without Aura: Evidence for Neurodegeneration?

Elevated S100B and Neuron Specific Enolase Levels in Patients with Migraine-without Aura: Evidence for Neurodegeneration?

Nramp1 gene affects selective early steps in macrophage-mediated anti-cryptococcal defense

A Transmissible Cytotoxic Activity Isolated from a Patient with Brain Ischemia Causes Microglial Cell Activation and Dysfunction

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