2026-10-14T05:33:42Z https://api.figshare.com/v2/oai

oai:figshare.com:article/34049258 2026-10-01T17:46:18Z category_4 category_8 category_12 category_15 category_16 category_39 category_46 category_734 category_132 category_134 portal_5 item_type_6 month_year_10_2026

<p>Kidney histopathology scoring criteria.</p> Kaitlyn Grando (12527650) Molly Elkins (9980979) Lauren Nicastro (25157996) Shingo Bessho (13257073) Sophia Olubajo (24393496) Anita Kowal (25157999) Vincent Tam (2583448) Roberto Caricchio (18920) David Pisetsky (5618543) Gregg J. Silverman (7949903) Çagla Tükel (45788) Biochemistry Microbiology Cell Biology Neuroscience Physiology Ecology Immunology Biological Sciences not elsewhere classified Infectious Diseases Virology specific elisa confirmed significantly affect proteinuria chromatin autoantibody responses div >< p systemic lupus erythematosus demonstrated increased anti f1 mice compared biofilms drive anti f1 mice previously demonstrated autoantibody levels prone mice older mice lpr mice young nzbxw treated controls study uncovers spontaneous disease salmonella </ prone nzbxw prominent feature often marked novel mechanism increasing morbidity either model disease stage disease flares coli </ autoimmune manifestations amyloidogenic protein already high <div><p>Systemic lupus erythematosus (SLE) is characterized by autoantibody production alongside inflammatory manifestations, including nephritis. In SLE, infections are frequent and associated with disease flares, increasing morbidity and mortality. Additionally, dysbiosis, often marked by overgrowth of Pseudomonadota, is a prominent feature of SLE and lupus nephritis. We previously demonstrated that complexes of DNA and curli, an amyloidogenic protein from biofilms of Pseudomonadota, including <i>Salmonella</i> Typhimurium and <i>E. coli</i>, can induce anti-dsDNA and anti-chromatin autoantibody responses. Here, we assessed the effects of curli administration or <i>Salmonella</i> infection on autoimmune manifestations in wild-type and lupus-prone mice. A multiplex autoantibody assay showed increased levels of anti-C1q antibodies in curli-treated C57BL/6 and lupus-prone NZBxW/F1 mice compared to PBS-treated controls. An anti-C1q-specific ELISA confirmed the presence of anti-C1q antibodies in C57BL/6 mice after treatment with curli/DNA, extracted from <i>E. coli</i> or <i>Salmonella</i> biofilms, or infection with <i>Salmonella</i>. Prior to the onset of spontaneous disease, sera from young NZBxW/F1 mice, injected with curli, demonstrated increased anti-dsDNA and anti-C1q antibody responses compared to PBS-treated controls; however, no differences were found in older mice, post-onset, when autoantibody levels were already high. In MRL/lpr mice, curli treatment significantly exacerbated anti-C1q antibody production regardless of age and disease stage, compared to PBS-treated controls. While curli treatment did not significantly affect proteinuria in either model, curli-treatment of MRL/lpr mice significantly increased C1q deposition in glomeruli. This study uncovers a novel mechanism for the induction of anti-C1q autoantibodies and how infection or dysbiosis may exacerbate renal disease in SLE.</p></div> 2026-10-01T17:56:08Z Text Journal contribution 10.1371/journal.ppat.1014666.s007 https://figshare.com/articles/journal_contribution/_p_XXX_p_/34049258 CC BY 4.0