PMID- 22496194
OWN - NLM
STAT- MEDLINE
DCOM- 20120720
LR  - 20220129
IS  - 1526-632X (Electronic)
IS  - 0028-3878 (Print)
IS  - 0028-3878 (Linking)
VI  - 78
IP  - 17
DP  - 2012 Apr 24
TI  - Increased muscle expression of interleukin-17 in Duchenne muscular dystrophy.
PG  - 1309-14
LID - 10.1212/WNL.0b013e3182518302 [doi]
AB  - OBJECTIVES: Duchenne muscular dystrophy (DMD) is a degenerative muscle wasting 
      disease caused by mutations in the dystrophin gene. Dystrophic muscle is 
      characterized by chronic inflammation, and inflammatory mediators could be 
      promising targets for innovative therapeutic interventions. We analyzed muscle 
      biopsy samples of DMD-affected children to characterize interleukin (IL)-17 and 
      Forkhead box P3 (Foxp3) expression levels and to identify possible correlations 
      with clinical status. METHODS: Expression levels of IL-17, Foxp3, tumor necrosis 
      factor-alpha (TNF-alpha), monocyte chemoattractant protein-1 (MCP-1), IL-6, and 
      transforming growth factor-beta (TGF-beta) were analyzed by real-time PCR in muscle 
      biopsy samples from patients with DMD (n = 27) and juvenile dermatomyositis (JDM) 
      (n = 8). Motor outcome of patients with DMD was evaluated by North Star 
      Ambulatory Assessment score. RESULTS: In DMD, we found higher levels of IL-17 and 
      lower levels of Foxp3 mRNA compared with those for a typical inflammatory 
      myopathy, JDM. Moreover, the IL-17/Foxp3 ratio was higher in DMD than in JDM 
      biopsy samples. IL-17 mRNA levels appeared to be related to the expression levels 
      of other proinflammatory cytokines (TNF-alpha and MCP-1) and significantly associated 
      with clinical outcome of patients. CONCLUSIONS: The association of IL-17 
      expression with levels of other inflammatory cytokines and with the clinical 
      course of DMD suggests a possible pathogenic role of IL-17.
FAU - De Pasquale, L
AU  - De Pasquale L
AD  - Division of Rheumatology, Bambino Gesu Children's Hospital, Rome, Italy.
FAU - D'Amico, A
AU  - D'Amico A
FAU - Verardo, M
AU  - Verardo M
FAU - Petrini, S
AU  - Petrini S
FAU - Bertini, E
AU  - Bertini E
FAU - De Benedetti, F
AU  - De Benedetti F
LA  - eng
GR  - GGP06119/TI_/Telethon/Italy
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120411
PL  - United States
TA  - Neurology
JT  - Neurology
JID - 0401060
RN  - 0 (Chemokine CCL2)
RN  - 0 (FOXP3 protein, human)
RN  - 0 (Forkhead Transcription Factors)
RN  - 0 (Interleukin-17)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Biopsy
MH  - Chemokine CCL2/metabolism
MH  - Child
MH  - Child, Preschool
MH  - Forkhead Transcription Factors/metabolism
MH  - Humans
MH  - Interleukin-17/*metabolism
MH  - Interleukin-6/metabolism
MH  - Muscle, Skeletal/*metabolism/pathology
MH  - Muscular Dystrophy, Duchenne/*metabolism
MH  - Reference Values
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - Up-Regulation
PMC - PMC3335450
EDAT- 2012/04/13 06:00
MHDA- 2012/07/21 06:00
PMCR- 2013/04/24
CRDT- 2012/04/13 06:00
PHST- 2012/04/13 06:00 [entrez]
PHST- 2012/04/13 06:00 [pubmed]
PHST- 2012/07/21 06:00 [medline]
PHST- 2013/04/24 00:00 [pmc-release]
AID - WNL.0b013e3182518302 [pii]
AID - WNL203643 [pii]
AID - 10.1212/WNL.0b013e3182518302 [doi]
PST - ppublish
SO  - Neurology. 2012 Apr 24;78(17):1309-14. doi: 10.1212/WNL.0b013e3182518302. Epub 
      2012 Apr 11.