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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>