Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration

By L. Qin, Xuefei Wu, M. Block, Yuxin Liu, G. Breese, Jau-Shyong Hong, D. Knapp, Fulton Crews. Glia, 2007

2,143 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/f046fcdb7db7063b1e22610d24db7edc09324177

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Citations in the corpus

The inflammatory & neurodegenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression (2009, background): “inflammation, reflected by activation of brain microglia with a chronically elevated production of pro-inflammatory mediators, such as TNFα, which may remain elevated for 10 months (Qin et al. 2007; Kent et al. 1992).”
Microglial Activation & Chronic Neurodegeneration (2010, methodology): “onstrate resolution of the innate immune response, as is common in the peripheral immune system.(156) Al-”
Alternatively activated microglia and macrophages in the central nervous system. (2015, background): “On the other hand, higher dosages of LPS (5–10 mg/kg; i.p.) are required to detect TNFa up-regulation in the CNS (Qin et al., 2007; Thompson et al., 2008).”
Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease (2011, background): “Interestingly, a single administration of LPS given to adult mice has been reported to cause progressive dopaminergic neuronal loss (Qin et al., 2007).”
Neuroinflammation and depression: A review (2020, background): “Moreover, it has been demonstrated that peripheral LPS challenge induces TNF-α synthesis in the liver and increases serum TNF-α, which then crosses the BBB to activate brain microglia and induce cytokines and other pro-inflammatory factors (Qin et al., 2007).”
Psychoneuroimmunology Meets Neuropsychopharmacology: Translational Implications of the Impact of Inflammation on Behavior (2012, background): “…endotoxin (5 mg/kg) to adult mice led to an almost 50% decrease in tyrosine hydroxylase-expressing neurons in the substantia nigra after 10 months (Qin et al, 2007), and chronic administration of high-dose endotoxin (2 weeks at 5 ng/h) into the brain was associated with a 70% reduction of nigral…”
Innate immunity and neuroinflammation in the CNS: The role of microglia in Toll‐like receptor‐mediated neuronal injury (2009, neutral): “GLIA of these cells (Monje et al., 2003; Qin et al., 2007).”
Microglia and neurodegeneration: The role of systemic inflammation (2013, background): “…despite reservations about the acute and severe nature of the initial stimulus in these studies, LPS has proved to induce apparently self-sustaining inflammation (Qin et al., 2007), and MPTP-induced inflammation has proved to have similar longevity in monkeys and in humans (Langston et al., 1999).”
Genomic Analysis of Reactive Astrogliosis (2012, methodology): “Although LPS itself mostly fails to cross the blood– brain barrier (Banks and Robinson, 2010), this treatment induces microglia activation in response to induction of inflammatory cytokines in the periphery (Buttini and Boddeke, 1995; Qin et al., 2007) that subsequently leads to astrocyte activation”
Cerebral Microglia Recruit Monocytes into the Brain in Response to Tumor Necrosis Factorα Signaling during Peripheral Organ Inflammation (2009, background): “Furthermore, the absence of TNF signaling was shown to significantly inhibit central inflammation in response to LPS induced systemic inflammation (Qin et al., 2007).”
Regulation of Tau Pathology by the Microglial Fractalkine Receptor (2010, positive): “w) LPS doses and that the latter dose produced neurodegeneration and chronic microglial activation, which could be observed 10 months postinjection (Qin et al., 2007).”
Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, positive): “PD is also recognized to have an inflammatory component (Qin et al., 2007).”