Sodium Chloride Aggravates Arthritis via Th17 Polarization
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Purpose: Sodium chloride (NaCl) has been proposed as a driving factor in autoimmune diseases through the induction of pathogenicCD4+ T helper cells that produce interleukin-17 (Th17 cells). This study investigated the effects of NaCl on inflammatory arthritisin mice and humans. Materials and Methods: Collagen-induced arthritis (CIA) mice were fed a normal or high-salt diet ad libitum, and clinical andhistologic features of arthritis were evaluated. The proportion of Th17 cells in the spleens of CIA mice fed a normal or high-saltdiet was evaluated by flow cytometry, and the expression of IL-17 in joints and intestines was determined by immunohistochemicalstaining. We also analyzed the effect of NaCl on Th17 differentiation from peripheral blood monocytes of patients with rheumatoidarthritis (RA) and osteoarthritis (OA) and evaluated the contents of sodium and IL-17 in the synovial fluid of RA and OApatients. Results: NaCl increased murine and human Th17 cell differentiation in a dose-dependent manner. Clinical and histological arthritiswas more severe in the high-salt-fed CIA mice, compared to control CIA mice. The proportion of Th17 cells among splenocyteswas higher in CIA mice fed a high-salt diet. Expression of synovial and intestinal IL-17 was also higher in high-salt-fed CIAmice. Comparison of synovial fluid between RA patients and OA patients revealed that Na+ and IL-17 were more abundant in RAsynovial fluid. Conclusion: This study suggests that NaCl can aggravate arthritis by affecting Th17 differentiation. Accordingly, limiting salt intakemay be helpful for treating inflammatory arthritis, such as RA.
Abstract
Purpose: Sodium chloride (NaCl) has been proposed as a driving factor in autoimmune diseases through the induction of pathogenicCD4+ T helper cells that produce interleukin-17 (Th17 cells). This study investigated the effects of NaCl on inflammatory arthritisin mice and humans. Materials and Methods: Collagen-induced arthritis (CIA) mice were fed a normal or high-salt diet ad libitum, and clinical andhistologic features of arthritis were evaluated. The proportion of Th17 cells in the spleens of CIA mice fed a normal or high-saltdiet was evaluated by flow cytometry, and the expression of IL-17 in joints and intestines was determined by immunohistochemicalstaining. We also analyzed the effect of NaCl on Th17 differentiation from peripheral blood monocytes of patients with rheumatoidarthritis (RA) and osteoarthritis (OA) and evaluated the contents of sodium and IL-17 in the synovial fluid of RA and OApatients. Results: NaCl increased murine and human Th17 cell differentiation in a dose-dependent manner. Clinical and histological arthritiswas more severe in the high-salt-fed CIA mice, compared to control CIA mice. The proportion of Th17 cells among splenocyteswas higher in CIA mice fed a high-salt diet. Expression of synovial and intestinal IL-17 was also higher in high-salt-fed CIAmice. Comparison of synovial fluid between RA patients and OA patients revealed that Na+ and IL-17 were more abundant in RAsynovial fluid. Conclusion: This study suggests that NaCl can aggravate arthritis by affecting Th17 differentiation. Accordingly, limiting salt intakemay be helpful for treating inflammatory arthritis, such as RA.
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