Abstract
(1) Background: Psoriatic Arthritis (PsA) is a painful disease of the joints and spine. Recent reports observed distinct enteric dysbiosis in PsA; intake of probiotic strains is considered to ameliorate enteric dysbiosis. If probiotics are effective in PsA is elusive. (2) Methods: In this pilot open-label study we enrolled 10 PsA patients with low to medium disease activity who received probiotics for 12 weeks. Analysis of faecal zonulin, α1-antitrypsin and calprotectin, as well as peripheral immune phenotyping was performed at baseline, after 12 weeks and 12 weeks after termination of probiotic intake. (3) Results: All patients showed increased levels of the enteric permeability marker zonulin which correlated with the frequency of peripheral Th17 cells. Calprotectin, a marker for intestinal inflammation was elevated in 6 out of 10 patients. Probiotic intake resulted in a reduction of disease activity and gut permeability. These effects, however, were not sustained beyond termination of probiotic intake. (4) Conclusions: PsA patients suffer from enhanced enteric permeability and inflammation. Probiotics may ameliorate disease activity in PsA by targeting these alterations.
Highlights
Psoriatic Arthritis (PsA) is the most prevalent coexisting condition of psoriasis affecting one third of the patients
PsA belongs to the family of spondyloarthritis (SpA) sharing features with ankylosing spondylitis, reactive arthritis and enteropathic arthritis
Patients visiting the rheumatology outpatient clinic were asked to participate in the study in case they met the inclusion criteria: (1) diagnosis of PsA diagnosed by a rheumatologist and satisfied CASPAR criteria, (2) low or moderate disease activity, (3) age above 18 years, (4) stable immunomodulatory therapy over
Summary
Psoriatic Arthritis (PsA) is the most prevalent coexisting condition of psoriasis affecting one third of the patients. SpA has been linked to bacterial triggers; the HLA-B27 transgenic rat model of SpA does not develop disease in a germ free environment [2]. SKG mice develop a PsA-like disease depending on the presence of bacterial colonization or injection of β-glycan, a polysaccharide found in bacterial and fungal cell walls. In this model CD4+ T-cell immune responses and interleukin-17 (IL-17) are involved in the development of arthritis [3,4]. IL-17 secreting CD4+ T-cells (Th17) physiologically fight bacterial and fungal infection.
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