Abstract
Mesenchymal stem/stromal cells (MSCs) have immunosuppressive and regenerative properties. Adipose tissue is an alternative source of MSCs, named adipose-derived mesenchymal stem cells (ASCs). Because the biology of ASCs in rheumatic diseases (RD) is poorly understood, we performed a basic characterization of RD/ASCs. The phenotype and expression of adhesion molecules (intracellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1) on commercially available healthy donors (HD), ASC lines (n = 5) and on ASCs isolated from patients with systemic lupus erythematosus (SLE, n = 16), systemic sclerosis (SSc, n = 17) and ankylosing spondylitis (AS, n = 16) were analyzed by flow cytometry. The secretion of immunomodulatory factors by untreated and cytokine-treated ASCs was measured by ELISA. RD/ASCs have reduced basal levels of CD90 and ICAM-1 expression, correlated with interleukin (IL)-6 and transforming growth factor (TGF)-β1 release, respectively. Compared with HD/ASCs, untreated and tumour necrosis factor (TNF) + interferon (IFN)-γ (TI)-treated RD/ASCs produced similar amounts of prostaglandin E2 (PGE2), IL-6, leukemia inhibiting factor (LIF), and TGF-β1, more IL-1Ra, soluble human leukocyte antigen G (sHLA-G) and tumor necrosis factor-inducible gene (TSG)-6, but less kynurenines and galectin-3. Basal secretion of galectin-3 was inversely correlated with the patient’s erythrocyte sedimentation rate (ESR) value. IFN-α and IL-23 slightly raised galectin-3 release from SLE/ASCs and AS/ASCs, respectively. TGF-β1 up-regulated PGE2 secretion by SSc/ASCs. In conclusion, RD/ASCs are characterized by low basal levels of CD90 and ICAM-1 expression, upregulated secretion of IL-1Ra, TSG-6 and sHLA-G, but impaired release of kynurenines and galectin-3. These abnormalities may modify biological activities of RD/ASCs.
Highlights
Rheumatic diseases (RD), triggered by a complex interplay of genetic and environmental factors and mediated by autoimmune and/or autoinflammatory mechanisms, are characterized by chronic inflammation, progressive damage and functional impairment of affected tissues and organs [1]
There were no significant differences between patient groups in body mass index (BMI), disease duration, and erythrocyte sedimentation rate (ESR) values, but Systemic lupus erythematosus (SLE) patients were younger than Systemic sclerosis (SSc) patients, and Ankylosing spondylitis (AS)
All AS patients were HLA-B27 positive and they were mostly treated with non-steroid anti-inflammatory drugs (NSAIDs)
Summary
Rheumatic diseases (RD), triggered by a complex interplay of genetic and environmental factors and mediated by autoimmune and/or autoinflammatory mechanisms, are characterized by chronic inflammation, progressive damage and functional impairment of affected tissues and organs [1]. Systemic lupus erythematosus (SLE) is a multisystemic disease of autoimmune background. Overactivation of B cells, production of numerous autoantibodies, and defective immunoregulation are pivotal in SLE pathogenesis [2]. Systemic sclerosis (SSc), a rare autoimmune disease, is characterized by vascular derangement, abnormal fibroblast activation and progressive multi-organ fibrosis [3]. In SSc and SLE, serious life-threatening manifestations are common. Ankylosing spondylitis (AS) is accompanied by inflammatory back pain, damage to joint structures, and pathological bone formation, leading to spine ankylosis
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