Astrocytes are active players in cerebral innate immunity

Farina, Cinthia; Aloisi, Francesca; Meinl, Edgar

doi:10.1016/j.it.2007.01.005

Cited by 1,144 publications

(1,042 citation statements)

References 100 publications

(112 reference statements)

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“…In general, astrocyte responses to chemokines involve chemotaxis, cell proliferation and survival (Farina et al, 2007). Increased levels of GFAP may also indicate astrocyte activation in our cell cultures by chronic CXCL10 treatment.…”

Section: Discussionmentioning

confidence: 89%

Chronic CXCL10 alters the level of activated ERK1/2 and transcriptional factors CREB and NF-κB in hippocampal neuronal cell culture

Bajova

Nelson

Gruol

2008

Journal of Neuroimmunology

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Signal transduction pathways may be important targets of chemokines during neuroinflammation. In the current study, Western blot analyses show that in rat hippocampal neuronal/glial cell cultures chronic CXCL10 increases the level of protein for ERK1/2 as well as for the transcriptional factors CREB and NF-κB. Bcl-2, an anti-apoptotic protein whose expression can be regulated by a pathway involving ERK1/2, CREB and NF-κB, was also increased in the CXCL10 treated cultures. These results implicate a role for ERK1/2, CREB and NF-κB in effects of CXCL10 on hippocampal cells and suggest that chronic CXCL10 may have a protective role during certain neuroinflammatory conditions.

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Section: Discussionmentioning

confidence: 89%

Chronic CXCL10 alters the level of activated ERK1/2 and transcriptional factors CREB and NF-κB in hippocampal neuronal cell culture

Bajova

Nelson

Gruol

2008

Journal of Neuroimmunology

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“…The IL-1R/TLR superfamily comprises cell surface PRRs sharing a conserved region termed the Toll/IL-1R (TIR) domain (O'Neill, 2008;O'Neill and Dinarello, 2000). Several TLRs are expressed in human astrocytes in vitro, including TLR2, TLR3, and TLR4 (Farina et al, 2007). However, whereas TLR3 shows consistent expression in the resting state, studies examining TLR2 and TLR4 expression in astrocytes have produced conflicting results, which may reflect differences in cell source and culture conditions (Crack and Bray, 2007;Farina et al, 2007;Kielian, 2006).…”

Section: Astrocytes As Source and Target Of Inflammatory Moleculesmentioning

confidence: 99%

“…Reactive astrocytes are a source of complement components and also express complement-regulatory proteins, as well as complement receptors [for review see (Farina et al, 2007); Fig. 1].…”

Section: Astrocytes As Source and Target Of Inflammatory Moleculesmentioning

confidence: 99%

“…However, over the past decade there has been accumulating evidence supporting the central role of astrocytes in the CNS innate immune response induced by a variety of insults. Astrocytes have been shown to initiate, regulate, and amplify immune-mediated mechanisms involved in different human CNS diseases, including epilepsy [for reviews see (Farina et al, 2007;Seifert et al, 2010)]. In this review we will largely focus on protoplasmic astrocytes that predominate in gray matter, and fibrous astrocytes that predominate in white matter.…”

mentioning

confidence: 99%

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Astrocyte immune responses in epilepsy

Aronica

Ravizza

Zurolo

et al. 2012

Glia

184

149

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Astrocytes, the major glial cell type of the central nervous system (CNS), are known to play a major role in the regulation of the immune/inflammatory response in several human CNS diseases. In epilepsy-associated pathologies, the presence of astrogliosis has stimulated extensive research focused on the role of reactive astrocytes in the pathophysiological processes that underlie the development of epilepsy. In brain tissue from patients with epilepsy, astrocytes undergo significant changes in their physiological properties, including the activation of inflammatory pathways. Accumulating experimental evidence suggests that proinflammatory molecules can alter glio-neuronal communications contributing to the generation of seizures and seizure-related neuronal damage. In particular, both in vitro and in vivo data point to the role of astrocytes as both major source and target of epileptogenic inflammatory signaling. In this context, understanding the astroglial inflammatory response occurring in epileptic brain tissue may provide new strategies for targeting astrocyte-mediated epileptogenesis. This article reviews current evidence regarding the role of astrocytes in the regulation of the innate immune responses in epilepsy. Both clinical observations in drug-resistant human epilepsies and experimental findings in clinically relevant models will be discussed and elaborated, highlighting specific inflammatory pathways (such as interleukin-1b/toll-like receptor 4) that could be potential targets for antiepileptic, disease-modifying therapeutic strategies. V

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“…CCL2 and its primary receptor CCR2 are also widely expressed within the central nervous system (CNS), implicating roles for CCL2 in the CNS as well as in the immune system (Ambrosini and Aloisi, 2004;Bajetto et al, 2002). Sources of CCL2 within the CNS include microglia and astrocytes, although some neurons can also produce CCL2 (Babcock et al, 2003;Banisadr et al, 2005a;Farina et al, 2007;Josselyn and Nguyen, 2005;Kielian et al., 2002;Weiss and Berman, 1998) Emerging evidence supports both physiological and pathological roles for CCL2 in the CNS. CCL2 expression in the normal CNS starts at an early stage of development, suggesting a physiological role for CCL2 in CNS development (Geppert, 2003;Meng et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells

Cho

Gruol

2008

Journal of Neuroimmunology

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Emerging evidence indicates that chemokines can regulate both the physiology and biochemistry of CNS neurons and glia. In the current study, Western blot analysis showed that in rat hippocampal neuronal/glial cultures the signal transduction pathway activated by CCL2, a chemokine expressed in the normal brain and at elevated levels during neuroinflammation, involves a G-protein coupled receptor, p38 MAPK as well as its immediate upstream kinase MKK3/6, and the downstream transcription factor CREB. ERK 1/2 and the transcription factors STAT1 and STAT3 do not play a prominent role. CCL2 also altered Ca 2+ influx and synaptic network activity in the hippocampal neurons. These results suggest an important role for p38 MAPK and CREB in hippocampal actions of CCL2.

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Astrocytes are active players in cerebral innate immunity

Cited by 1,144 publications

References 100 publications

Chronic CXCL10 alters the level of activated ERK1/2 and transcriptional factors CREB and NF-κB in hippocampal neuronal cell culture

Chronic CXCL10 alters the level of activated ERK1/2 and transcriptional factors CREB and NF-κB in hippocampal neuronal cell culture

Astrocyte immune responses in epilepsy

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells

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