2019
DOI: 10.1186/s12974-019-1538-9
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Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR4/NF-kB pathway

Abstract: Background Neuroinflammation is the response of the central nervous system to events that interfere with tissue homeostasis and represents a common denominator in virtually all neurological diseases. Activation of microglia, the principal immune effector cells of the brain, contributes to neuronal injury by release of neurotoxic products. Toll-like receptor 4 (TLR4), expressed on the surface of microglia, plays an important role in mediating lipopolysaccharide (LPS)-induced microglia activation an… Show more

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Cited by 365 publications
(231 citation statements)
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“…astrocytes [47], which maintain central sensitization and mechanical hyperalgesia [48]. In addition, activation of NMDA receptor in the spinal cord dorsal horn is one of key events, driving central sensitization and pain hypersensitivity [49].…”
Section: Discussionmentioning
confidence: 99%
“…astrocytes [47], which maintain central sensitization and mechanical hyperalgesia [48]. In addition, activation of NMDA receptor in the spinal cord dorsal horn is one of key events, driving central sensitization and pain hypersensitivity [49].…”
Section: Discussionmentioning
confidence: 99%
“…Toll-like receptor 4 (TLR4) is a congenital immune receptor expressed in hepatocytes. When LPS enters the liver, it synergizes with TLR4 and ultimately causes nuclear factor-κB (NF-κB) translocation, which is a highly conserved and tightly regulated signaling pathway central to liver survival and homeostasis that regulates the expression of inflammatory factors and induces liver inflammation (Porras et al, 2017;Zusso et al, 2019). Overall, the LPS-TLR4-NF-κB pathway is not only a bridge between the intestinal homeostasis and liver inflammation, but also provides the possibility to reduce liver diseases by protecting intestinal function (Chassaing et al, 2014).…”
Section: Introductionmentioning
confidence: 99%
“…Activation of the NF-κB signaling pathway can induce expression of the proinflammatory cytokines IL-6 [13], TNF-α, and IL-1β [14], and these proinflammatory factors can further activate NF-κB, thus aggravating inflammation [15]. IL-6, TNF-α and IL-1β are important cytokines secreted by cells used to evaluate the inflammatory response.…”
Section: Discussionmentioning
confidence: 99%