Abstract
We aimed to characterize the salivary protein components and identify biomarkers in patients with systemic lupus erythematosus (SLE). A proteomic analysis using two-dimensional gel electrophoresis and mass spectrometry was performed to determine the alterations of salivary proteins between patients with SLE and healthy controls, and the concentrations of the candidate proteins were measured through Western blot analysis and the enzyme-linked immunosorbent assay. The 10 differentially expressed protein spots were immunoglobulin gamma-3 chain C region (IGHG3), immunoglobulin alpha-1 chain C region, protein S100A8, lactoferrin, leukemia-associated protein 7, and 8-oxoguanine DNA glycosylase. The patients with SLE exhibited enhanced salivary IGHG3 (3.9 ± 2.15 pg/mL) and lactoferrin (4.7 ± 1.8 pg/mL) levels compared to patients with rheumatoid arthritis (1.8 ± 1.01 pg/mL and 3.2 ± 1.6 pg/mL, respectively; p < 0.001 for both) or healthy controls (2.2 ± 1.64 pg/mL and 2.2 ± 1.7 pg/mL, respectively; p < 0.001 for both). The salivary IGHG3 levels correlated with the erythrocyte sedimentation rate (r = 0.26, p = 0.01), anti-double-stranded DNA (dsDNA) antibody levels (r = 0.25, p = 0.01), and nephritis (r = 0.28, p = 0.01). The proteomic analysis revealed that the salivary IGHG3 levels were associated with SLE and lupus disease activity, suggesting that salivary IGHG3 may be a promising noninvasive biomarker for SLE.
Highlights
Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease characterized by the production of pathogenic autoantibodies and an aberrant inflammatory response leading to diverse clinical manifestations [1]
The salivary IGHG3 levels correlated with the erythrocyte sedimentation rate (ESR), antidsDNA antibody, lupus nephritis (LN), and immunosuppresssants in patients with systemic lupus erythematosus (SLE)
The aberrant expression of Fcγ receptor (FcγR) for IgG was observed in patients with SLE, and FcγR is involved in antigen presentation, the maturation of dendritic cells, and plasma cell survival in SLE [21]
Summary
Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease characterized by the production of pathogenic autoantibodies and an aberrant inflammatory response leading to diverse clinical manifestations [1]. The disease status of SLE, including clinical manifestations and disease activity, varies with the progression of the disease. Anti-double-stranded DNA (dsDNA) antibody and complement protein levels are used as the markers for diagnosis or monitoring of SLE [2,3]. The activation of a complement system leads to the consumption or depletion of complement proteins during SLE disease flares [8]. The low levels of complements 3 and 4 have been used as a diagnostic or a disease activity marker in SLE [1]. Complement proteins are not a reliable indicator of active SLE status sometimes, as their concentrations vary widely, and the complement protein level does not indicate the consumption in the tissue or the presence of an anticomplement autoantibody [9]. Several candidates, such as cytokines, immune cells, autoantibodies, or genetic markers, have been identified as potential biomarkers for SLE
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