Serum C-C Motif Ligand 11/eotaxin-1 May Serve as a Candidate Biomarker for Postmenopausal Osteoporosis.

Background: The chemokine C-C motif ligand 11, also known as eotaxin-1, has been identified as a novel mediator of inflammatory bone resorption. However, little is known regarding a potential role for CCL11/Eotaxin-1 in postmenopausal osteoporosis.

Objective: The scope of this study was to explore the relationship between serum CCL11/Eotaxin-1 concentrations and disease progression of postmenopausal females with osteoporosis.

Methods: A total of 83 postmenopausal women diagnosed with osteoporosis were enrolled. Meanwhile, 82 postmenopausal women with normal bone mineral density (BMD) and 85 healthy controls inner child-bearing age were enrolled as control. The Dual-energy X-ray absorptiometry was used to examine the BMDs at the femoral neck, lumbar spine 1-4 and total hip of all participants. Serum CCL11/Eotaxin-1 levels were examined by enzyme-linked immunosorbent assay. We also included inflammation marker interleukin-6 (IL-6) as well as a serum marker of bone resorption C-telopeptide cross-linked collagen type 1 (CTX-1). The Visual Analogue Scale (VAS) and Oswestry Disability Index (ODI) were recorded to evaluate the clinical severity in POMP females.

Results: Serum CCL11/Eotaxin-1 levels were significantly elevated in postmenopausal osteoporotic patients PMOP patients compared with PMNOP and healthy controls. We observed a significant negative correlation of serum CCL11/Eotaxin-1 levels with lumbar spine, femoral neck and total hip BMD. Furthermore, serum CCL11/ Eotaxin-1 concentrations were also positively related to the VAS and ODI scores. Last, serum CCL11/ Eotaxin-1 concentrations were positively associated with IL-6 and CTX-1 levels. These correlations remain significant after adjusting for age and BMI. Multivariate linear regression analysis demonstrated that CCL11/Eotaxin-1 could serve as an independent marker.

Conclusions: Serum CCL 11/Eotaxin-1 may serve as a candidate biomarker for postmenopausal osteoporosis. Therapeutics targeting CCL11/Eotaxin-1 and its related signalling way to prevent and slow progression of PMOP deserve further study.