Thus, using different serotypes of LPS and their different application routes may cause different outcomes. LPS from many Gram-negative bacteria species initiates acute inflammatory responses in mammals and induces a diverse range of effects, ranging from pyrexia to Gram-negative septic shock. LPS is found in the outer membrane of Gram-negative bacteria and acts as endotoxin. The history of understanding LPS starts in the late nineteenth century. Over the last two decades, studies in animal models have demonstrated that inflammation induced by lipopolysaccharide (LPS) can replicate some characteristics of PD, including extensive activation of microglia and selective loss of dopaminergic neurons in the nigrostriatal system. Therefore, it is essential to study the inflammatory process in PD, which may help us understand the pathogenesis of the disease and eventually develop an effective therapeutic strategy. Importantly, clinical researches have reported that microglial activation was found in the nigrostriatal system of PD patients. This microglial-neuronal interaction will be reinforced and become a self-amplifying cycle of neuronal injury and microglial activation, which finally leads to more neuronal damage and death. Additionally, damaged neurons may emit injury signals to cause microglia activation, which used to be defined as reactive microgliosis. However, uncontrolled activated microglia produces a variety of neurotoxic factors such as proinflammatory cytokines (interleukin-1 (IL-1), tumor necrosis factor alpha (TNF- α), interleukin-6 (IL-6)), nitro oxide (NO), prostaglandin E2, and superoxide, which lead to neuronal damage or death. Activated microglia can serve diverse beneficial functions essential to neuron survival, which include cellular maintenance and innate immunity. In response to various pathogenic stimuli including inflammation, microglia are readily activated and undergo a transformation to amoeboid morphology with an upregulated catalogue of surface molecules. Typically microglia exist in a resting state characterized by ramified morphology and monitor the brain environment. In the central nervous system, microglia, the resident innate immune cells, play a major role in the inflammatory process. Recently, inflammatory processes have been implicated as one of the active contributors to dopaminergic neuron damage in the development and progression of the disease. Although the etiology and pathogenesis of PD remain not fully elucidated, many interacting pathological processes appear to contribute to dopaminergic neuron degeneration in the disease. In PD, clinical symptoms including tremor, rigidity, and bradykinesia are primarily resulted from the loss of dopamine-containing neurons in the substantia nigra pars compacta. Parkinson's disease (PD) is the most prevalent neurodegenerative movement disorder.
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