Serum and CSF levels of MCP-1 and IP-10 in multiple sclerosis patients with acute and stable disease and undergoing immunomodulatory therapies

Franciotta, Diego; Martino, Gianvito; Zardini, Elisabetta; Furlan, Roberto; Bergamaschi, Roberto; Andreoni, Laura; Cosi, V.

doi:10.1016/s0165-5728(01)00261-2

Cited by 158 publications

(122 citation statements)

References 21 publications

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“…Recently accumulated evidence has demonstrated an elevated serum IP-10 level in various diseases, including inflammatory disease, and has shown its utility as a clinically useful biomarker. [13][14][15] For instance, Tang et al 16 demonstrated that IP-10 is an independent predictor of outcome for severe acute respiratory syndrome patients. Another group has demonstrated elevated IP-10 levels in patients with coronary artery disease.…”

Section: Discussionmentioning

confidence: 99%

Serum levels of the Th1 chemoattractant interferon-gamma-inducible protein (IP) 10 are elevated in patients with essential hypertension

Stumpf

Auer

Yılmaz³

et al. 2011

Hypertens Res

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Growing evidence shows that inflammation has a pivotal role in the pathophysiology of essential hypertension (EH). Although it has been acknowledged that target organ damage involves an inflammatory response, most work has focused on the role of macrophages, but T lymphocytes have recently become the center of interest. The goal of our study was to evaluate the role of T-cell-specific cytokines in the pathogenesis of EH. The study examined 39 patients with EH (57.7±6.8 years, systolic blood pressure (SBP) 157.5 ± 11.8 mm Hg, diastolic blood pressure 92.2 ± 12.9 mm Hg, mean arterial pressure 113.9 ± 12.6 mm Hg) and 30 healthy, normotensive controls (55.2 ± 4.9 years). Blood was drawn from a peripheral vein, and serum levels of interferon-inducible protein (IP)-10 and interleukins (IL)-4, -7 and -13 were measured by a multiplexing assay. Hypertensive patients had significantly higher levels of IP-10, IL-4, IL-7 and IL-13 than control subjects. When the patients were classified into tertiles according to their serum IP-10 levels (T1: 41.2-94.1 pg ml À1 ; T2: 103.4-162.5 pg ml À1 ; T3: 171.7-443.5 pg ml À1 ), the patients classified into the highest tertile also had the highest blood pressure. In a correlation analysis, plasma IP-10 concentration was significantly associated with SBP (r¼0.59, Po0.001). Furthermore, hypertensives with microalbuminuria, an early sign of hypertensive target organ damage, had the highest IP-10 levels. A stepwise multivariate regression analysis revealed IP-10 as the strongest independent predictor of SBP (P¼0.01). In conclusion, our study provides new insights into the pathophysiological mechanisms in EH linking inflammation and IP-10. However, these preliminary results need to be confirmed in larger trials.

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Section: Discussionmentioning

confidence: 99%

Serum levels of the Th1 chemoattractant interferon-gamma-inducible protein (IP) 10 are elevated in patients with essential hypertension

Stumpf

Auer

Yılmaz³

et al. 2011

Hypertens Res

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“…These data indicate that MCP-1 is one of the major proinflammatory cytokines. In the central nervous system, MCP-1 was detected in the serum and CSF of patients with multiple sclerosis and the ischemic stroke (Franciotta et al, 2001;Losy and Zaremba, 2001). Previous studies have reported that MCP-1 deficiency in genetically altered mice and the nonpeptide C-C chemokine receptor antagonist TAK-779 reduced infarct volume and macrophage accumulations in the stroke model (Hughes et al, 2001;Takami et al, 2002), and that anti-MCP-1-neutralizing antibody attenuated N-methyl-D-aspartate-induced brain injury in the striatum and hippocampus (Galasso et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Anti—Monocyte Chemoattractant Protein-1 Gene Therapy Protects against Focal Brain Ischemia in Hypertensive Rats

Kumai

Ooboshi

Takada

et al. 2004

J Cereb Blood Flow Metab

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Summary:Monocyte chemoattractant protein-1 (MCP-1) is expressed in the ischemic cortex after focal brain ischemia and appears to exacerbate ischemic damage. The authors examined the effect of gene transfer of dominant negative MCP-1, called 7ND, 90 minutes after induction of focal brain ischemia in hypertensive rats. Adenoviral vectors encoding mutant MCP-1 (Ad7ND; n ‫ס‬ 11), or Escherichia coli ␤-galactosidase (AdlacZ; n ‫ס‬ 17) as control were injected into the lateral ventricle of male spontaneously hypertensive rats. Both AdlacZ (n ‫ס‬ 12) and Ad7ND (n ‫ס‬ 6) administration provided transgene expression as early as 6 hours after injection and the expression further increased on day 1, followed by a sustained detection on day 5. Five days after ischemia, infarct volume (75 ± 13 mm 3 , n ‫ס‬ 5, mean ± SD) significantly reduced to 72% of control (104 ± 22 mm 3 , n ‫ס‬ 5, P < 0.05) by 7ND gene transfer. Numbers of leukocytes in the vessels (48.3 ± 32.9/cm 2 ) and macrophage/monocyte infiltration (475.2 ± 125.5 /mm 2 ) of the infarct area in the Ad7ND group were significantly less than those measured in the AdlacZ group (143.8 ± 72.1/cm 2 and 671.8 ± 125.5/mm 2 , P < 0.05, respectively). In summary, the postischemic gene transfer of dominant negative MCP-1 attenuated the infarct volume and infiltration of inflammatory cells, suggesting potential usefulness of the anti-MCP-1 gene therapy.

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“…The CXC chemokine ligand 10 (CXCL10) is thought to play an important role in neuroinflammatory diseases and its action may involve neuronal cells (van Marle et al, 2004). During CNS neuroinflammation expression of CXCL10 is elevated several fold (Franciotta et al, 2001;Kieseier et al, 2002;Kolb et al, 1999;Letendre et al, 1999;Sorensen et al, 1999;Xia et al, 2000) and occurs in a variety of CNS cells including astrocytes, microglia, and neurons (Asensio and Campbell, 1999;Carter et al, 2007;Kutsch et al, 2000;Ransohoff et al, 1993;Rossi and Zlotnik, 2000;Shen et al, 2006;Simpson et al, 2000;Wang et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

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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Serum and CSF levels of MCP-1 and IP-10 in multiple sclerosis patients with acute and stable disease and undergoing immunomodulatory therapies

Cited by 158 publications

References 21 publications

Serum levels of the Th1 chemoattractant interferon-gamma-inducible protein (IP) 10 are elevated in patients with essential hypertension

Serum levels of the Th1 chemoattractant interferon-gamma-inducible protein (IP) 10 are elevated in patients with essential hypertension

Anti—Monocyte Chemoattractant Protein-1 Gene Therapy Protects against Focal Brain Ischemia in Hypertensive Rats

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

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