Leukotrienes in patients with clinically active multiple sclerosis

Neu, I.; Metzger, Gérard; Zschocke, Johannes; Zelezny, R.; Mayatepek, Ertan

doi:10.1034/j.1600-0404.2002.00070.x

Cited by 29 publications

(38 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As discussed above (see section II.D), the beneficial effects on EAE after either genetic or pharmacological BLT 1 R targeting (Fretland et al, 1991;Gladue et al, 1996;Kihara et al, 2010) suggest that that BLT 1 R signaling may potentially affect both the onset and severity of MS. In support of this, increased levels of LTB 4 have been detected in cerebrospinal fluid from patients with MS (Neu et al, 1992(Neu et al, , 2002. Of interest, 5-LO was identified as one of the most up-regulated genes by microarray analysis in both human MS lesions and in brains from mice after EAE induction (Whitney et al, 2001).…”

Section: F Potential Therapeutic Applicationsmentioning

confidence: 82%

International Union of Basic and Clinical Pharmacology. LXXXIV: Leukotriene Receptor Nomenclature, Distribution, and Pathophysiological Functions

Bäck¹,

Dahlén²,

Drazen³

et al. 2011

Pharmacol Rev

130

View full text Add to dashboard Cite

Section: F Potential Therapeutic Applicationsmentioning

confidence: 82%

International Union of Basic and Clinical Pharmacology. LXXXIV: Leukotriene Receptor Nomenclature, Distribution, and Pathophysiological Functions

Bäck¹,

Dahlén²,

Drazen³

et al. 2011

Pharmacol Rev

130

View full text Add to dashboard Cite

“…There have been contradictory reports regarding the change of leukotriene levels in MS patients and animal models. Some studies found that the LTB4 and LTC4 levels are significantly increased in the cerebrospinal fluid (CSF) of MS patients compared with the controls [117,118]. But no significant difference exists in LTC4 production between MS and control peripheral blood monocytes and macrophages [118,119].…”

Section: Leukotriene Receptorsmentioning

confidence: 99%

G protein-coupled receptors as therapeutic targets for multiple sclerosis

Xie

2012

Cell Res

View full text Add to dashboard Cite

G protein-coupled receptors (GPCRs) mediate most of our physiological responses to hormones, neurotransmitters and environmental stimulants. They are considered as the most successful therapeutic targets for a broad spectrum of diseases. Multiple sclerosis (MS) is an inflammatory disease that is characterized by immune-mediated demyelination and degeneration of the central nervous system (CNS). It is the leading cause of non-traumatic disability in young adults. Great progress has been made over the past few decades in understanding the pathogenesis of MS. Numerous data from animal and clinical studies indicate that many GPCRs are critically involved in various aspects of MS pathogenesis, including antigen presentation, cytokine production, T-cell differentiation, T-cell proliferation, T-cell invasion, etc. In this review, we summarize the recent findings regarding the expression or functional changes of GPCRs in MS patients or animal models, and the influences of GPCRs on disease severity upon genetic or pharmacological manipulations. Hopefully some of these findings will lead to the development of novel therapies for MS in the near future.

show abstract

“…The 5-LOX gene was found to be a top risk gene in EAE (24). The brain concentrations of 5-LOX products, LTB 4 and LTD 4 , were upregulated (18,(22)(23), and favored the migration of inflammatory cells and lymphocytes in the brain of EAE mice (36)(37)(38). In the cuprizone model, the brain expression of 5-LOX was highly increased (39).…”

Section: Arachidonic Acid Pathway Activation In Animal Models Of Multmentioning

confidence: 99%

Pathogenesis and Progression of Multiple Sclerosis: The Role of Arachidonic Acid–Mediated Neuroinflammation

Palumbo

2017

Multiple Sclerosis: Perspectives in Treatment and Pathogenesis

View full text Add to dashboard Cite

Multiple sclerosis is characterized by inflammatory processes occurring within the central nervous system. In multiple sclerosis, inflammation could be either a physiological response secondary to the immune system activation or a phenomenon triggered by primary cytodegeneration of neurons and/ or oligodendrocytes without the involvement of immune cells. The arachidonic acid metabolism is activated via cyclooxygenases (COXs) and lipoxygenases (LOXs) in postmortem brain samples and in the cerebrospinal fluid of multiple sclerosis patients. It has been hypothesized that the arachidonic acid-mediated neuroinflammation could play a role in the pathogenic mechanisms triggering demyelination, oligodendrocyte loss, axonal pathology and, ultimately, motor dysfunctions, which are hallmarks of multiple sclerosis. COX-2 and 5-LOX selective inhibitors efficiently inhibit each of the hallmarks mentioned above in different animal models of multiple sclerosis. Thus, it is suggested that the arachidonic acid pathway represents a potential pharmacological target to ameliorate multiple sclerosis pathology and symptoms.

show abstract

Leukotrienes in patients with clinically active multiple sclerosis

Abstract: The increased concentration of LTB4 in the CSF of MS patients may indicate a biological importance for this mediator in MS.

Cited by 29 publications

References 18 publications

International Union of Basic and Clinical Pharmacology. LXXXIV: Leukotriene Receptor Nomenclature, Distribution, and Pathophysiological Functions

International Union of Basic and Clinical Pharmacology. LXXXIV: Leukotriene Receptor Nomenclature, Distribution, and Pathophysiological Functions

G protein-coupled receptors as therapeutic targets for multiple sclerosis

Pathogenesis and Progression of Multiple Sclerosis: The Role of Arachidonic Acid–Mediated Neuroinflammation

Contact Info

Product

Resources

About