The role of monocyte chemoattractant protein MCP1/CCL2 in neuroinflammatory diseases

Conductier, Grégory; Blondeau, Nicolas; Guyon, Alice; Nahon, Jean‐Louis; Rovère, Carole

doi:10.1016/j.jneuroim.2010.05.010

Cited by 348 publications

(281 citation statements)

References 102 publications

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“…These secreted inflammatory mediators, in turn, activate more microglia and astrocytes to produce inflammatory molecules. In addition, immune cells including, T cells, B cells and monocytes are found to migrate from the periphery through the BBB and present in the brains of AD individuals (Conductier et al 2010;Ruan et al 2010;Savarin-Vuaillat and Ransohoff 2007).…”

Section: Inflammation In Admentioning

confidence: 99%

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

Zhang

et al. 2015

Arch. Immunol. Ther. Exp.

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Alzheimer's disease (AD) is a complex agerelated neurodegenerative disorder of the central nervous system. Since the first description of AD in 1907, many hypotheses have been established to explain its causes. The inflammation theory is one of them. Pathological and biochemical studies of brains from AD individuals have provided solid evidence of the activation of inflammatory pathways. Furthermore, people with long-term medication of anti-inflammatory drugs have shown a reduced risk to develop the disease. After three decades of genetic study in AD, dozens of loci harboring genetic variants influencing inflammatory pathways in AD patients has been identified through genome-wide association studies (GWAS). The most well-known GWAS risk factor that is responsible for immune response and inflammation in AD development should be APOE e4 allele. However, a growing number of other GWAS risk AD candidate genes in inflammation have recently been discovered. In the present study, we try to review the inflammation in AD and immunity-associated GWAS risk genes like HLA-DRB5/DRB1, INPP5D, MEF2C, CR1, CLU and TREM2.

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Section: Inflammation In Admentioning

confidence: 99%

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

Zhang

et al. 2015

Arch. Immunol. Ther. Exp.

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“…10E). MCP-1 has been shown to play an important role in several neuroinflammatory diseases (57). However, in a study of 481 Thai patients with malaria, MCP-1 gene polymorphisms were not associated with CM (58) and in the murine model of ECM, MCP-1 expression in the brain did not differ between susceptible versus resistant strains of mice (59).…”

Section: Figurementioning

confidence: 99%

The Transcription Factor T-bet Regulates Parasitemia and Promotes Pathogenesis duringPlasmodium bergheiANKA Murine Malaria

Oakley

Sahu

Lotspeich-Cole

et al. 2013

The Journal of Immunology

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The pathogenesis of experimental cerebral malaria (ECM) is an immunologic process, mediated in part by Th1 CD4+ T cells. However, the role of the Th1 CD4+ T cell differentiation program on the ability to control parasitemia and susceptibility to ECM disease during blood stage malaria has never been assessed directly. Using the Plasmodium berghei ANKA murine model of ECM and mice deficient for the transcription factor T-bet (the master regulator of Th1 cells) on the susceptible C57BL/6 background, we demonstrate that although T-bet plays a role in the regulation of parasite burden, it also promotes the pathogenesis of ECM. T-bet−deficient (Tbx21−/−) mice had higher parasitemia than wild type controls did during the ECM phase of disease (17.7 ± 3.1% versus 10.9 ± 1.5%). In addition, although 100% (10/10) of wild type mice developed ECM by day 9 after infection, only 30% (3/10) of Tbx21−/− mice succumbed to disease during the cerebral phase of infection. Resistance to ECM in Tbx21−/− mice was associated with diminished numbers of IFN-γ–producing CD4+ T cells in the spleen and a lower accumulation of CD4+ and CD8+ T cells in the brain. An augmented Th2 immune response characterized by enhanced production of activated GATA-3+ CD4+ T cells and elevated levels of the eotaxin, MCP-1, and G-CSF cytokines was observed in the absence of T-bet. Our results suggest that in virulent malarias, immune modulation or therapy resulting in an early shift toward a Th2 response may help to ameliorate the most severe consequences of malaria immunopathogenesis and the prospect of host survival.

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“…6 It was found that CCL2 and its high-affinity receptor CCR2 could be involved directly in nociceptive signal transduction in neurons or glia.…”

Section: Discussionmentioning

confidence: 99%

“…4,5 For a long time, inflammatory CCL2 was thought to be involved specifically in the hematological system and in immune responses. 6 Although it is almost absent from the normal central nervous system, expression of CCL2 in the spinal cord could be induced following ischemia, neural trauma, and inflammation. [7][8][9][10][11] Similar up-regulation of CCL2 has also been found in the dorsal root ganglion (DRG) subjected to peripheral nerve injury.…”

Section: Introductionmentioning

confidence: 99%

Chemokine ligand 2 in the trigeminal ganglion regulates pain induced by experimental tooth movement

Yang

Luo

Wang

et al. 2014

The Angle Orthodontist

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Objective: To test the hypothesis that the chemokine ligand 2/chemokine receptor 2 (CCL2/ CCR2) signaling pathway plays an important role in pain induced by experimental tooth movement. Materials and Methods: Expression of CCL2/CCR2 in the trigeminal ganglion (TG) was determined by Western blotting 0 hours, 4 hours, 1 day, 3 days, 5 days, and 7 days after tooth movement. CCL2 localization and cell size distribution were revealed by immunohistochemistry. The effects of increasing force on CCL2 expression and behavioral changes were investigated. Furthermore, the effects of CCL2/CCR2 antagonists on these changes in pain behaviors were all evaluated. Exogenous CCL2 was injected into periodontal tissues and cultured TG neurons with different concentrations, and then the pain responses or c-fos expression were assessed. Results: Experimental tooth movement led to a statistically significant increase in CCL2/CCR2 expression from day 3 to day 7, especially in small to medium-sized TG neurons. It also triggered an increase in the time spent on directed face-grooming behaviors in a force magnitudedependent and CCL2 dose-dependent manner. Pain induced by experimental tooth movement was effectively blocked by a CCR2 antagonist and by CCL2 neutralizing antibody. Also, exogenous CCL2 led to an increase in c-fos expression in cultured TG neurons, which was blocked by CCL2 neutralizing antibody. Conclusions: The peripheral CCL2/CCR2 axis is modulated by experimental tooth movement and involved in the development of tooth movement pain. (Angle Orthod. 2014;84:730-736.)

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The role of monocyte chemoattractant protein MCP1/CCL2 in neuroinflammatory diseases

Cited by 348 publications

References 102 publications

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

The Transcription Factor T-bet Regulates Parasitemia and Promotes Pathogenesis duringPlasmodium bergheiANKA Murine Malaria

Chemokine ligand 2 in the trigeminal ganglion regulates pain induced by experimental tooth movement

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