Abstract
Objective This study aimed to estimate serum IL-17A and Claudin-1 levels, investigate their correlation, and evaluate their diagnostic significance as potential blood-based biomarkers in psoriasis. Methods Serum IL-17A and Claudin-1 concentrations were determined using enzyme-linked immunosorbent assay (ELISA). Statistical analyses were performed to determine differences in serum levels of IL-17A and Claudin-1, their bivariable correlation with psoriasis severity, as Psoriasis Area Severity Index (PASI), and their predictive abilities using receiver operating characteristic (ROC) curves. Results Significantly higher IL-17A and lower Claudin-1 levels were found in psoriasis (p < 0.05). PASI did not correlate significantly with either IL-17A or Claudin-1 in psoriasis and their subtypes. The only significant correlation between serum IL-17A and Claudin-1 was shown in late-onset psoriasis (r = 0.630, p = 0.028). ROC curve analysis indicated the serum IL-17A, serum Claudin-1, and combination of IL-17A and serum Claudin-1 for predicting psoriasis with the areas under the curve (AUC) of 0.951 (p < 0.0001), 0.709 (p = 0.0119), and 0.949 (p < 0.0001), respectively. Moreover, the potential role in distinguishing between early-onset and late-onset psoriasis: we obtained serum IL-17A, serum Claudin-1, and their combination AUC of 0.590 (p = 0.3126), 0.741 (p = 0.0045), and 0.741 (p = 0.0067), respectively. However, none of the serum IL-17A, serum Claudin-1, and their combination was well-performed discriminating mild psoriasis from moderate-to-severe psoriasis with AUC of 0.553 (p = 0.5596), 0.518 (p = 0.8539), and 0.559 (p = 0.5225), respectively. Conclusion These preliminary results suggest that the serum Claudin-1 as a potential biomarker and the relationship and possible regulatory interactions between IL-17A and Claudin-1 in psoriasis are distinguishable by age of onset.
Highlights
Psoriasis is a multifactorial chronic, immune-mediated, inflammatory, systemic dermatosis of complex pathogenesis including genetic, environmental, and immunological factors [1]. e classic psoriatic morphology of erythematous scaly plaques is histopathologically due to hyperkeratosis, parakeratosis, acanthosis, angiogenesis, and perivascular lymphohistiocytic infiltrate
Differential Expression of Serum IL-17A and Claudin-1 in Psoriasis. e results of comparative analysis on serum levels of IL-17A and Claudin-1 are presented in Supplementary Table 2 and Figure 1, and show a significant difference between the psoriatic patients (IL-17A: 20.88 ± 0.31, range 17.12–25.16; Claudin-1: 327.00 ± 33.00, range 15.98–880.01, respectively) and healthy controls (IL-17A: 13.12 ± 0.88, range 7.52–20.76; Claudin-1: 538.82 ± 85.12, range 60.62–1428.69, respectively) with the Mann–Whitney U test (IL-17A, p ≤ 0.001; Claudin-1, p 0.006; Figures 1(a) and 1(d))
We found that the association of serum IL-17A and Claudin-1 was significant in early/late-onset psoriasis; inconsistently, some studies reported no difference and others a significant difference in several other diseases, in animal models of other diseases and in cellular models of other diseases. e question whether IL-17A regulates Claudin-1 remains unanswered; findings that they are correlated should be met with caution: further prospective studies are required, especially in psoriasis. erefore, we speculate on the role of IL-17A on Claudin-1, which may contribute to new therapeutic approaches
Summary
Psoriasis is a multifactorial chronic, immune-mediated, inflammatory, systemic dermatosis of complex pathogenesis including genetic, environmental, and immunological factors [1]. e classic psoriatic morphology of erythematous scaly plaques is histopathologically due to hyperkeratosis, parakeratosis, acanthosis, angiogenesis, and perivascular lymphohistiocytic infiltrate. Psoriasis coexists with both physical and psychiatric multimorbidity, which leads to high disease burden, morbidity, and mortality [2]. It approximately affects 60 million adults worldwide and cannot currently be cured [3]. Immunological mechanism of the centrality of IL-17A, the shooting target of the therapeutic “hierarchy,” have been identified as key drivers of psoriasis pathogenesis and psoriasis multimorbidity [4]. Psoriasis has long been associated with skin barrier dysregulation [6], in which tight junction (TJ), as an important component in epidermal barrier function, is seen to be clearly altered in psoriasis [7,8]. There is little consensus on Claudin-1 patterns in psoriatic skin. The Contrast Media & Molecular Imaging significance of serum Claudin-1 in psoriasis is not known yet. erefore, the etiopathogenesis of psoriasis still needs to be studied
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