Abstract
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with multiple autoantibody production and often affects the kidneys, known as lupus nephritis. However, the mechanism underlying lupus nephritis development is unclear. Biofilms that protect bacteria from stress are ubiquitous in almost every environment. Here, we identified that a conserved peptide (HU1) derived from DNABII proteins, one of major bacterial biofilm components, was specifically recognized by sera from about 47% patients with SLE. Moreover, the serum anti-HU1 levels showed a significant positive correlation with lupus nephritis occurrence. Presence of antibodies against HU1 in pristane-induced mice aggravated lupus nephritis, although these antibodies also attenuated bacterial biofilm formation. We further identified that antibodies against HU1 cross-recognized protein disulfide isomerase (P4HB) located on the renal cell surface and inhibited the activities of this enzyme. Our findings reveal a novel mechanism underlying the development of lupus nephritis triggered by bacterial biofilms.
Highlights
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the presence of numerous autoantibodies and immune complex formation [1]
As bacterial biofilms in vivo are directly exposed to the human immune system and DNABII proteins are the major DNA binding proteins in biofilms, we examined whether these conserved proteins could trigger immune responses
We determined the presence of antibodies against these DNABII proteins in patients with rheumatoid arthritis (RA), SLE and primary Systemic sclerosis and in healthy donors by Enzyme linked immunosorbent assay (ELISA)
Summary
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the presence of numerous autoantibodies and immune complex formation [1]. Lupus nephritis (LN) is characterized by renal deposition of immune complexes and considered as a major risk factor for morbidity and mortality in SLE [2]. Deposition of autoantibody and immune complexes in renal compartments contributes to the development of LN, the pathogenesis of LN is far from clear [3]. Both genetic and environmental triggers contribute to SLE [4]. Bacterial infection is an important environmental trigger for lupus onset as well as the leading cause of morbidity and
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