The involvement of galectin-3 in skin injury in systemic lupus erythematosus patients

Abstract

Objective Our previous research suggested that anti-galectin-3 antibody was highly associated with the development of lupus skin lesions in systemic lupus erythematosus (SLE). In this study we aimed to investigate the involvement of galectin-3 in SLE skin damage. Methods The study consisted of 49 patients with SLE, 16 with dermatomyositis and 11 with systemic scleroderma and 20 healthy controls. Galectin-3 was examined by ELISA and immunohistochemical staining in serum and skin, respectively. Results Serum galectin-3 was significantly higher in patients with SLE than in those with dermatomyositis ( P < 0.01), systemic scleroderma ( P < 0.001) and healthy controls ( P < 0.001); however, it was comparable between SLE patients with and without skin lesions ( P = 0.2010 and was not correlated with cutaneous disease activity ( r = -0.020, P = 0.93) or damage score ( r = -0.380, P = 0.09). Galectin-3 expression was reduced in epidermis in lesional skin from patients with SLE, dermatomyositis and systemic scleroderma compared to healthy controls ( P = 0.0055), whereas it was comparable among diseases ( P > 0.05). As for subtypes of skin lesions in SLE, galectin-3 expression was lower in chronic cutaneous lupus erythematosus than in acute cutaneous lupus erythematosus ( P = 0.0439). Conclusion Serum galectin-3 is unlikely to play a role in the pathogenesis of lupus skin damage, but can be a potential biomarker for the measurement of SLE disease activity. Galectin-3 is greatly reduced in patients with lupus lesions compared with healthy controls, which may contribute to the recruitment of inflammatory cells in the skin.

Serum galectin-3 and galectin-3 binding protein levels in systemic lupus erythematosus and cutaneous lupus erythematosus

“…Interestingly, in the present study we found that in patients with SLE there was no difference in Gal-3 concentration in groups with and without LE-specific skin lesions. Similar results were obtained by Shi et al in 2018 [9]. It is noteworthy that in the present study we noted for the first time that patients with SLE with and without skin lesions did not differ in G3BP levels.…”

“…Clinical and laboratory characteristics of patients with systemic lupus erythematosus with lupus-specific skin lesions, systemic lupus erythematosus without lupus-specific skin lesions and discoid lupus erythematosus (NA -not available). P-value in one row shows statistical differences between 2 or 3 values depending on characteristic down resulted in the overexpression of chemokines such as CXCL1 and CCL20, and enhanced the peripheral blood mononuclear cell-attracting capacity of keratinocytes [9]. It is worth mentioning that purified anti-Gal-3 antibodies administered subcutaneously to mice resulted in LE histopathological changes (vasculitis and epidermal atrophy) [21].…”

“…Interestingly, serum Gal-3 and G3BP proteins were much higher in SLE than in Behcet's disease and healthy groups [8]. The results of further studies revealed that Gal-3 and G3BP concentrations were elevated in the sera of SLE patients compared to healthy controls [9][10][11][12][13][14]. However, by reason of the pioneering character of the research as well as the small number of the study groups, their role as markers of the immune and inflammatory processes in SLE requires further investigation.…”

Plasma galectin‐3 levels do not differ in systemic lupus erythematosus patients

“…Recently, the correlation between galectin‐3 and the pathogenesis of autoimmune diseases has been demonstrated . Moreover, 2 studies showed that galectin‐3 may be correlated with complement 3 and 4 levels and anti‐double‐stranded DNA (anti‐dsDNA) in SLE . In addition, a recent study showed that the pathogenesis of SLE‐related skin injuries may be closely related to anti‐galectin‐3 antibodies, but evidence of the association between clinical manifestations of SLE and galectin‐3 remains limited.…”

“…may be correlated with complement 3 and 4 levels and anti-doublestranded DNA (anti-dsDNA) in SLE. 8,9 In addition, a recent study showed that the pathogenesis of SLE-related skin injuries may be closely related to anti-galectin-3 antibodies, 10 but evidence of the association between clinical manifestations of SLE and galectin-3 remains limited.…”