TLR2 and Parkinson disease: Enteroendocrine cells express receptors for bacterial-derived components (toll-like receptors, TLR), and they respond to TLR agonists with increased proinflammatory cytokine production.27-30 Two studies have implicated a TLR-mediated response to bacterial ligands in Parkinson’s disease pathogenesis.31 TLR4 knockout mice exhibit attenuated motor dysfunction and neuro- and gastrointestinal inflammation and neurodegeneration in response to rotenone treatment.32 TLR2-deficient α-synuclein-overexpressing mice were found to have less neurodegeneration and neuronal α-synuclein concentrations.33