Involvement of Mitochondrial Dysfunction in the Inflammatory Response in Human Mesothelial Cells from Peritoneal Dialysis Effluent.

Recent studies have related mitochondrial impairment with peritoneal membrane damage during peritoneal dialysis (PD) therapy. Here, we assessed the involvement of mitochondrial dysfunction in the inflammatory response in human mesothelial cells, a hallmark in the pathogenesis of PD-related peritoneal membrane damage. Our ex vivo studies showed that IL-1β causes a drop in the mitochondrial membrane potential in cells from peritoneal effluent.

Mitochondrial Dysfunction and Oxidative Stress in Rheumatoid Arthritis.

Control of excessive mitochondrial oxidative stress could provide new targets for both preventive and therapeutic interventions in the treatment of chronic inflammation or any pathology that develops under an inflammatory scenario, such as rheumatoid arthritis (RA). Increasing evidence has demonstrated the role of mitochondrial alterations in autoimmune diseases mainly due to the interplay between metabolism and innate immunity, but also in the modulation of inflammatory response of resident cells, such as synoviocytes. Thus, mitochondrial dysfunction derived from several danger signals could activate tricarboxylic acid (TCA) disruption, thereby favoring a vicious cycle of oxidative/mitochondrial stress.

Clinical significance of high levels of soluble tumour necrosis factor-α receptor-2 produced by alternative splicing in rheumatoid arthritis: a longitudinal prospective cohort study.

Objectives: We investigated whether serum levels of an alternatively spliced soluble (s)TNF receptor-2 (DS-TNFR2) affected the clinical response to anti-TNF-α therapy, classical DMARDs or radiological evidence of disease progression in patients with RA.

Methods: We included 116 patients with RA. Cohort 1: 52 DMARD-naïve early RA patients [mean (s.

[Evidence of inflammatory mechanisms in osteoarthritis].

Classically, osteoarthritis (OA) is not considered an inflammatory arthropathy, because of the presence of a small number of neutrophils in the synovial fluid and the absence of systemic manifestations of inflammation. Besides, the characteristics of articular cartilage (avascular, alymphatic and aneural) do disable to fulfill with the classical signs of inflammation (redness, swelling, heat, pain). However, thanks to development of molecular and cellular biology, there are multiple studies which shown that different proinflammatory mediators, such as the cytokines IL-1β and TNFα, could be important in the development of this disease.