“…When the highly toxic exudates of enterotoxigenic strains of B. fragilis escape the microbial-dense environment of the human GI-tract they can produce substantial systemic inflammatory pathology with significant mortality and morbidity. B. fragilis proliferation and excess is associated with the development of multiple pro-inflammatory bowel cancers, bacteremia, brain and intra-abdominal abscess, cellulitis, colitis, diabetic ulcer, diarrhea, necrotizing fasciitis, peritonitis, sepsis, septicemia, systemic infection and systemic inflammation, the development of neurological diseases involving progressive, age-related inflammatory neurodegeneration (such as AD), and those neurological disorders that display a significantly elevated incidence of atypical developmental programming against a background of aging (such as schizophrenia) [37,[70][71][72][73][74][75][76]. Very recently LPS-induced systemic inflammation has been associated with synaptic loss and cognitive decline in multiple human neurological disorders and in transgenic murine models for AD, and a role for LPS-mediated microglial release of pro-inflammatory cytokines, such as interleukin IL-1β, is currently based on both in vivo and primary culture studies in vitro [53,73].…”