Multiple Sclerosis, 1 May 2002, vol. 8, no. 3, pp. 222-228(7)
Liuzzi GM[1]; Trojano M[2]; Fanelli M[3]; Avolio C[4]; Fasano A[1];
Livrea P[2]; Riccio P[5]
[1] Department of Biochemistry and Molecular Biology, University of
Bari, Bari, Italy [2] Department of Neurology and Psychiatric Sciences,
University of Bari, Bari, Italy [3] Department of Hygiene, University of
Bari, Bari, Italy [4] Chair of Neurology, University of Foggia, Italy [5]
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