Immune-Neuroendocrine Dysregulation in Patients with Osteoarthritis: A Revision and a Pilot Study

Abstract

An immune-neuroendocrine dysregulation affecting both systemic inflammatory and stress mediators and the function of innate immune cells underlies OA. This reflects an altered feedback between the innate/inflammatory and stress responses in this pathology.

Analysis of gene expression and methylation datasets identified ADAMTS9, FKBP5, and PFKBF3 as biomarkers for osteoarthritis

“…Besides, researchers also found that immune complexes and immunoglobulins against cartilage components were detected in the synovium, plasma, and cartilage of patients with OA (Qian et al, ). Further studies confirmed that immune‐neuroendocrine dysregulation in OA could affect systemic inflammatory, stress mediators, and the function of innate immune cells, making it meaningful to investigate the pathophysiological mechanisms of immune response and inflammatory response in the development of OA (Gálvez et al, ). Apoptosis and inflammation of chondrocytes are one of the most important mechanisms in the pathogenesis of OA.…”

Innate/inflammatory bioregulation and clinical effectiveness of whole-body hyperthermia (balneotherapy) in elderly patients with osteoarthritis

“…The neutrophils' phagocytic capacity against opsonized bacteria (Staphylococcus epidermidis) was evaluated by flow cytometry of heparinized whole blood. This quantitative technique allows the evaluation of the percentage of active 'phagocytic neutrophils' and the number of bacteria ingested per cell by measuring the mean fluorescence intensity (MFI) of active phagocytic cells, which reflects the phagocytic activity of neutrophils [8]. In brief, bacteria were stained with fluorescein isothiocyanate (FITC) (1 lg/ml) and opsonized with human serum.…”

“…In addition to local inflammatory events occurring within joint tissues such as the release of inflammatory mediators by cartilage, bone and synovium [4,5], low-grade systemic inflammation also plays a pivotal role in this condition. The presence of low-grade systemic inflammation could lead to the initiation and aggravation of OA, whereas locally produced inflammatory mediators, such as cytokines, might be reflected in peripheral blood and contribute to perpetuate this systemic inflammatory status [6][7][8]. Patients with OA also present changes in peripheral blood T cell composition [9].…”

“…Patients with OA also present changes in peripheral blood T cell composition [9]. Furthermore, they have an immune-neuroendocrine dysregulation affecting the negative feedback between the inflammatory and stress responses along with the decreased functional capacity of phagocytes, thus reflecting an altered bioregulation of the innate/inflammatory responses and suppression of the immune system's defenses against pathogens [8].…”

“…Thus, our main objective was to evaluate the participation of regulatory T (Treg) cells in the anti-inflammatory effects of mud therapy in elderly OA patients. In contrast, and taking into account our previous observations of a reduced neutrophil-mediated innate immune response in patients with OA [8], the second objective was to assess whether the innate immune cell function is affected by the anti-inflammatory effects of this intervention. In addition, we examined the correlation between concentrations of systemic inflammatory cytokines and clinical outcomes of the OA patients after the intervention.…”