“…A working hypothesis is that in non-lupus-prone individuals, or murine strains, natural infections do not normally result in the systemic release of curli-DNA composites in amount equivalent to those we injected in this study; while in susceptible individuals, genetically determined dysfunctions may increase the systemic exposure to curli-DNA composites during chronic infections. The more frequent outcome of Salmonella infection in bacteremia and complications in soft tissues in SLE patients (Lim et al, 2001; Pablos et al, 1994; Tsao et al, 2002) and the recent identification of increased levels of circulating endotoxin in SLE patients (Shi et al, 2014), support this hypothesis. In addition, since inflammatory cytokines can decrease intestinal mucosal barrier function (Turner, 2009), the high levels of cytokines present in pre-disease stages of lupus (Connolly and Hakonarson, 2012; Sriram et al, 2012), might compromise mucosal barrier function and allow the biofilm material produced by microbiota at mucosal sites to access the immune system, act as danger signals and trigger lupus onset.…”