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Neuropeptides CRH, SP, HK-1, and Inflammatory Cytokines IL-6 and TNF Are
Increased in Serum of Patients with Fibromyalgia Syndrome, Implicating Mast
Cells
#MMPMID26763911
Tsilioni I
; Russell IJ
; Stewart JM
; Gleason RM
; Theoharides TC
J Pharmacol Exp Ther
2016[Mar]; 356
(3
): 664-72
PMID26763911
show ga
Fibromyalgia syndrome (FMS) is a chronic, idiopathic condition of widespread
musculoskeletal pain affecting more women than men. Even though clinical studies
have provided evidence of altered central pain pathways, the lack of definitive
pathogenesis or reliable objective markers has hampered development of effective
treatments. Here we report that the neuropeptides corticotropin-releasing hormone
(CRH), substance P (SP), and SP-structurally-related hemokinin-1 (HK-1) were
significantly (P = 0.026, P < 0.0001, and P = 0.002, respectively) elevated (0.82
± 0.57 ng/ml, 0.39 ± 0.18 ng/ml, and 7.98 ± 3.12 ng/ml, respectively) in the
serum of patients with FMS compared with healthy controls (0.49 ± 0.26 ng/ml,
0.12 ± 0.1 ng/ml, and 5.71 ± 1.08 ng/ml, respectively). Moreover, SP and HK-1
levels were positively correlated (Pearson r = 0.45, P = 0.002) in FMS. The serum
concentrations of the inflammatory cytokines interleukin (IL)-6 and tumor
necrosis factor (TNF) were also significantly (P = 0.029 and P = 0.006,
respectively) higher (2.97 ± 2.35 pg/ml and 0.92 ± 0.31 pg/ml, respectively) in
the FMS group compared with healthy subjects (1.79 ± 0.62 pg/ml and 0.69 ± 0.16
pg/ml, respectively). In contrast, serum IL-31 and IL-33 levels were
significantly lower (P = 0.0001 and P = 0.044, respectively) in the FMS patients
(849.5 ± 1005 pg/ml and 923.2 ± 1284 pg/ml, respectively) in comparison with
healthy controls (1281 ± 806.4 pg/ml and 3149 ± 4073 pg/ml, respectively). FMS
serum levels of neurotensin were not different from controls. We had previously
shown that CRH and SP stimulate IL-6 and TNF release from mast cells (MCs). Our
current results indicate that neuropeptides could stimulate MCs to secrete
inflammatory cytokines that contribute importantly to the symptoms of FMS.
Treatment directed at preventing the secretion or antagonizing these elevated
neuroimmune markers, both centrally and peripherally, may prove to be useful in
the management of FMS.
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