Contributions
Abstract: EP1492
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 15 Immunology
Vascular inflammation has been shown to be involved in conditions that promote chronic systemic inflammation, such as obesity, cancer, autoimmune and infectious diseases. Vascular inflammation is regulated by endothelial adhesion molecules, chemokines and inflammasome components that are expressed mostly by endothelial cells and pericytes. In this study, we aimed to analyze the significance of serum and cerebrospinal fluid (CSF) levels of vascular inflammation parameters in pathogenesis and development of multiple sclerosis (MS).
A total of 19 relapsing remitting MS (RRMS) patients, 18 clinically isolated syndrome (CIS) patients and 20 healthy controls were recruited for this study. Patients were in remission and were not under immunosuppressive treatment during serum and CSF sampling. Disease durations, EDSS scores, relapse numbers and oligoclonal band (OCB) status of all patients were recorded. Serum and CSF levels of tissue inhibitor of metalloproteinases-3 (TIMP3), matrix metallopeptidase 9 (MMP9), a disintegrin and metalloproteinase domain-containing protein 15 (ADAM15), platelet derived growth factor-BB (PDGF-BB), NOD-like receptor protein 1 (NLRP1) and NLRP3 were measured by ELISA.
There were no significant differences between serum and CSF levels of CIS and RRMS patients by means of vascular inflammation parameters, while both groups had higher levels of all parameters as compared to healthy controls. CSF but not serum PDGF-BB, MMP9, NLRP1 and NLRP3 levels of OCB positive RRMS patients were significantly higher than those of OCB negative patients. There was no correlation between serum/CSF vascular inflammation parameters and clinical-demographic features of RRMS patients.
Vascular inflammation appears to be activated as early as during the first MS attack. However, levels of vascular inflammation parameters are not altered in a time- or disability-dependent manner and thus cannot be used as indicators of MS conversion or as a prognostic biomarker. Increased CSF levels of OCB positive patients might be due to enhanced blood-brain barrier permeability and subsequently increased transport of myeloid cells or glial cell activation.
Disclosure:
Recai Türkoğlu: nothing to disclose
Murat Kürtüncü: nothing to disclose
Mefkure Eraksoy: nothing to disclose
Erdem Tüzün: nothing to disclose.
Abstract: EP1492
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 15 Immunology
Vascular inflammation has been shown to be involved in conditions that promote chronic systemic inflammation, such as obesity, cancer, autoimmune and infectious diseases. Vascular inflammation is regulated by endothelial adhesion molecules, chemokines and inflammasome components that are expressed mostly by endothelial cells and pericytes. In this study, we aimed to analyze the significance of serum and cerebrospinal fluid (CSF) levels of vascular inflammation parameters in pathogenesis and development of multiple sclerosis (MS).
A total of 19 relapsing remitting MS (RRMS) patients, 18 clinically isolated syndrome (CIS) patients and 20 healthy controls were recruited for this study. Patients were in remission and were not under immunosuppressive treatment during serum and CSF sampling. Disease durations, EDSS scores, relapse numbers and oligoclonal band (OCB) status of all patients were recorded. Serum and CSF levels of tissue inhibitor of metalloproteinases-3 (TIMP3), matrix metallopeptidase 9 (MMP9), a disintegrin and metalloproteinase domain-containing protein 15 (ADAM15), platelet derived growth factor-BB (PDGF-BB), NOD-like receptor protein 1 (NLRP1) and NLRP3 were measured by ELISA.
There were no significant differences between serum and CSF levels of CIS and RRMS patients by means of vascular inflammation parameters, while both groups had higher levels of all parameters as compared to healthy controls. CSF but not serum PDGF-BB, MMP9, NLRP1 and NLRP3 levels of OCB positive RRMS patients were significantly higher than those of OCB negative patients. There was no correlation between serum/CSF vascular inflammation parameters and clinical-demographic features of RRMS patients.
Vascular inflammation appears to be activated as early as during the first MS attack. However, levels of vascular inflammation parameters are not altered in a time- or disability-dependent manner and thus cannot be used as indicators of MS conversion or as a prognostic biomarker. Increased CSF levels of OCB positive patients might be due to enhanced blood-brain barrier permeability and subsequently increased transport of myeloid cells or glial cell activation.
Disclosure:
Recai Türkoğlu: nothing to disclose
Murat Kürtüncü: nothing to disclose
Mefkure Eraksoy: nothing to disclose
Erdem Tüzün: nothing to disclose.