Body fat has regulatory functions through producing cytokines and
adipokines whose role in the pathogenesis of Systemic Sclerosis (SSc) is
currently emerging. Changes in body mass, either overweight or
underweight status, entail a dysregulation of the cytokines/adipokines
network that may impact on SSc disease activity. We evaluated serum
levels of adipokines and cytokines in SSc patients and correlated them
to clinical features and body mass index (BMI) categories. The study
included 89 SSc patients and 26 healthy donors (HD). Serum levels of
adiponectin, leptin, resistin, visfatin, TNFα, IFNγ, IL-2, IL-10, and
IL-17A were measured by Multiplex Immunoassay, and correlated to BMI,
waist to hip ratio, and disease specific features. Mann-Whitney U-test
or t-Student for unpaired data, Kruskal-Wallis test or ANOVA, were used
for comparisons between groups. Spearman’s or Pearson’s test were used
for correlation analysis. Serum levels of TNFα, IL-2, leptin, and
resistin, were significantly higher in SSc than in HD. The highest
levels of IL-17A, IL-2, IL-10, leptin and visfatin were detected in
obese SSc patients (p <0.01). Conversely, underweight SSc
patients showed the highest TNFα levels (p<0.05), which were
negatively correlated with BMI (p=0.05). No correlation between
adipokines/cytokines and clinical characteristics was found. Adipokines,
IL-2, IL-10 and IL-17A were found to be increased in obese SSc patients,
but whether they play a role in the pathogenesis of the disease remains
to be investigated. Intriguingly, underweight patients had higher TNFα
levels, suggesting a potential role of TNFα in inducing the cachexia
observed in long-lasting disease.
NLRP1 influences the systemic sclerosis phenotype: a new clue for the contribution of innate immunity in systemic sclerosis-related fibrosing alveolitis pathogenesis
