PMID- 17439900
OWN - NLM
STAT- MEDLINE
DCOM- 20070613
LR  - 20151119
IS  - 1352-4585 (Print)
IS  - 1352-4585 (Linking)
VI  - 13
IP  - 3
DP  - 2007 Apr
TI  - Production of brain-derived neurotrophic factor by mononuclear cells of patients 
      with multiple sclerosis treated with glatiramer acetate, interferon-beta 1a, and 
      high doses of immunoglobulins.
PG  - 313-31
AB  - Sixty, relapsing remitting (RR) multiple sclerosis (MS) patients, who underwent 
      treatment with glatiramer acetate (GA), interferon (IFN)-beta 1a, and 
      immunoglobulins (Igs) (20 per treatment group), were assessed for levels of 
      brain-derived neurotrophic factor (BDNF) in the supernatants of unstimulated and 
      stimulated peripheral blood mononuclear cells (PBMCs) in the first year of 
      treatment. Phytohemagglutinin (PHA), anti-OKT3 antibody, myelin basic protein 
      (MPB) and GA were used as stimuli. Cytokine responses by ELISPOT and 
      lymphoproliferative responses were also assessed. The GA-treated MS patient group 
      showed a progressive increase in BDNF levels, from baseline to month three; 
      thereafter, the levels remained stable and significantly greater compared with 
      baseline and controls (ANOVA=P<0.001). IFN-beta 1a had no effect on BDNF 
      production, whereas Igs induced a slight decrease (ANOVA=P<0.04). ELISPOT 
      analysis revealed a significant decrease of IFN-gamma, an increase of interleukin 
      (IL)-4 and IL-5 in GA-treated MS patients, and an increase of IL-10 in patients 
      treated with IFN-beta 1a and GA. No significant correlation was found between 
      BDNF secretion in the supernatants of PBMCs and cytokine response, lesional load, 
      and measures of atrophy. Increased BDNF production related to GA treatment can 
      have implications for understanding the mechanism of action of this 
      immunomodulatory agent, in light of evidence suggesting its effects in promoting 
      neuroprotective immunity in MS patients; however, a clinically measurable effect, 
      especially in terms of an impact on actual disease progression, remains to be 
      established.
FAU - Sarchielli, P
AU  - Sarchielli P
AD  - Neurologic Clinic, Department of Medical and Surgical Specialties and Public 
      Health, University of Perugia, Perugia 06158, Italy. neuro.pg@tiscalinet.it
FAU - Zaffaroni, M
AU  - Zaffaroni M
FAU - Floridi, A
AU  - Floridi A
FAU - Greco, L
AU  - Greco L
FAU - Candeliere, A
AU  - Candeliere A
FAU - Mattioni, A
AU  - Mattioni A
FAU - Tenaglia, S
AU  - Tenaglia S
FAU - Di Filippo, M
AU  - Di Filippo M
FAU - Calabresi, P
AU  - Calabresi P
LA  - eng
PT  - Controlled Clinical Trial
PT  - Journal Article
DEP - 20070129
PL  - England
TA  - Mult Scler
JT  - Multiple sclerosis (Houndmills, Basingstoke, England)
JID - 9509185
RN  - 0 (Adjuvants, Immunologic)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Immunoglobulins)
RN  - 0 (Peptides)
RN  - 5M691HL4BO (Glatiramer Acetate)
RN  - 77238-31-4 (Interferon-beta)
RN  - XRO4566Q4R (Interferon beta-1a)
SB  - IM
MH  - Adjuvants, Immunologic/therapeutic use
MH  - Adult
MH  - Brain/anatomy & histology/pathology
MH  - Brain-Derived Neurotrophic Factor/*blood
MH  - Female
MH  - Follow-Up Studies
MH  - Glatiramer Acetate
MH  - Humans
MH  - Immunoglobulins/*therapeutic use
MH  - Interferon beta-1a
MH  - Interferon-beta/*therapeutic use
MH  - Leukocytes, Mononuclear/drug effects/*physiology
MH  - Lymphocyte Activation
MH  - Lymphocyte Count
MH  - Magnetic Resonance Imaging
MH  - Male
MH  - Multiple Sclerosis, Relapsing-Remitting/*blood/*drug therapy
MH  - Peptides/*therapeutic use
MH  - Time Factors
EDAT- 2007/04/19 09:00
MHDA- 2007/06/15 09:00
CRDT- 2007/04/19 09:00
PHST- 2007/04/19 09:00 [pubmed]
PHST- 2007/06/15 09:00 [medline]
PHST- 2007/04/19 09:00 [entrez]
AID - 1352458506070146 [pii]
AID - 10.1177/1352458506070146 [doi]
PST - ppublish
SO  - Mult Scler. 2007 Apr;13(3):313-31. doi: 10.1177/1352458506070146. Epub 2007 Jan 
      29.