Multiple Sclerosis, 1 May 2002, vol. 8, no. 3, pp. 222-228(7)
Liuzzi GM; Trojano M; Fanelli M; Avolio C; Fasano A; Livrea P; Riccio P
 Department of Biochemistry and Molecular Biology, University of Bari, Bari, Italy  Department of Neurology and Psychiatric Sciences, University of Bari, Bari, Italy  Department of Hygiene, University of Bari, Bari, Italy  Chair of Neurology, University of Foggia, Italy  Department of Biology D.B.A.F., University of Basilicata, Potenza, Italy
Matrix metalloproteinase-9 (MMP-9) was detected by zymography and enzyme-linked immunosorbent assay (ELISA) in matched serum and cerebrospinal fluid (CSF) samples from patients with neurological diseases.
Patients with relapsing-remitting multiple sclerosis (RR-MS) had serum and CSF MMP-9 levels comparable to those from patients with inflammatory neurological diseases (INDs), but higher than patients with non-inflammatory neurological diseases (NINDs) and healthy donors (HDs).
MMP-9 increased in active RR-MS in comparison with inactive RR-MS implying that MMP-9 in MS is related with clinical disease activity.
A correlation between the CSF/serum albumin (QAlb) and CSF/serum MMP-9 (QMMP-9) was observed in IND and NIND but not in RR-MS patients, indicating that CSF MMP-9 levels in NIND and IND patients could be influenced by serum MMP-9 and blood-brain barrier (BBB) permeability properties.
MS patients had higher values of QMMP-9:QAlb (MMP-9 index) than IND and NIND patients suggesting that in MS the increase in CSF MMP-9 could be due to intrathecal synthesis of MMP-9.
A significant inverse correlation was found between MMP-9 and its endogenous inhibitor TIMP-1 in RR-MS indicating that in MS patients both the increase in MMP-9 and the decrease in TIMP-1 serum levels could contribute to BBB disruption and T-lymphocyte entry into the CNS.
© 2002 ingenta