PMID- 12508404
OWN - NLM
STAT- MEDLINE
DCOM- 20030513
LR  - 20081121
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 30
IP  - 1
DP  - 2003 Jan
TI  - Detection of interleukin 1beta (IL-1beta), IL-6, and tumor necrosis factor-alpha 
      in skin of patients with fibromyalgia.
PG  - 146-50
AB  - OBJECTIVE: To determine if abnormal collagen metabolism is correlated with 
      neurogenic inflammation, a potential activator of collagen metabolism, in 
      patients with fibromyalgia (FM). METHODS: The presence of inflammatory cytokines, 
      interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-a was investigated 
      in skin tissues by using reverse transcription-polymerase chain reaction (RT-PCR) 
      and immunohistochemistry. Fifty-three skin biopsies from female patients with FM 
      (30-65 years of age) were examined and compared to skin biopsies of 10 age and 
      sex matched healthy controls. Biopsies were obtained from the left deltoid 
      region. Rheumatoid arthritis synovial fibroblasts and tissues were used as 
      positive controls for the expression of cytokines. Total RNA isolated from the 
      tissue samples were reverse transcribed (RT) by random hexamers as the primer for 
      RT followed by PCR amplification using specific primers for IL-1beta, IL-6 or 
      TNF-a. Expression of IL-1beta, and TNF-a protein was investigated in the skin by 
      immunohistochemistry using specific antibodies (avidin-biotin method). RESULTS: 
      Positive signals (RT-PCR) were detected in skin tissues of 19/50 (38%) FM 
      patients for IL-1beta, in 14/51 FM patients (27%) for IL-6, and in 17/53 patients 
      (32%) for TNF-a. None of the cytokines could be detected in healthy control skin. 
      Immunoreactivity for IL-1beta and TNF-a was demonstrated in certain skin tissues 
      of our FM patients. CONCLUSION: The detection of cytokines in FM skin indicates 
      the presence of inflammatory foci (neurogenic inflammation) in the skin of 
      certain patients (about 30% of FM patients), suggesting an inflammatory component 
      in the induction of pain. This may explain the response to nonsteroidal 
      antiinflammatory therapy in a subset of FM patients.
FAU - Salemi, Souzan
AU  - Salemi S
AD  - Center of Experimental Rheumatology, Department of Rheumatology and Institute of 
      Physical Medicine, University Hospital, Zurich, Switzerland .
FAU - Rethage, Janine
AU  - Rethage J
FAU - Wollina, Uwe
AU  - Wollina U
FAU - Michel, Beat A
AU  - Michel BA
FAU - Gay, Renate E
AU  - Gay RE
FAU - Gay, Steffen
AU  - Gay S
FAU - Sprott, Haiko
AU  - Sprott H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adult
MH  - Biopsy
MH  - Cytokines/analysis/*genetics
MH  - Female
MH  - Fibromyalgia/immunology/pathology/*physiopathology
MH  - Gene Expression/immunology
MH  - Humans
MH  - Immunohistochemistry
MH  - Interleukin-1/analysis/genetics
MH  - Interleukin-6/analysis/genetics
MH  - Middle Aged
MH  - RNA, Messenger/analysis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Skin/chemistry/immunology/pathology
MH  - Skin Physiological Phenomena/*immunology
MH  - Tumor Necrosis Factor-alpha/analysis/genetics
EDAT- 2003/01/01 04:00
MHDA- 2003/05/14 05:00
CRDT- 2003/01/01 04:00
PHST- 2003/01/01 04:00 [pubmed]
PHST- 2003/05/14 05:00 [medline]
PHST- 2003/01/01 04:00 [entrez]
AID - 0315162X-30-146 [pii]
PST - ppublish
SO  - J Rheumatol. 2003 Jan;30(1):146-50.