DOI . ORG {
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We began analyzing https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0149136, but it redirected us to https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0149136. The analysis below is for the second page.
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Description:
Survivors of sepsis often experience long-term cognitive and functional decline. Previous studies utilizing lipopolysaccharide injection and cecal ligation and puncture in rodent models of sepsis have demonstrated changes in depressive-like behavior and learning and memory after sepsis, as well as evidence of myeloid inflammation and cytokine expression in the brain, but the long-term course of neuroinflammation after sepsis remains unclear. Here, we utilize cecal ligation and puncture with greater than 80% survival as a model of sepsis. We found that sepsis survivor mice demonstrate deficits in extinction of conditioned fear, but no acquisition of fear conditioning, nearly two months after sepsis. These cognitive changes occur in the absence of neuronal loss or changes in synaptic density in the hippocampus. Sepsis also resulted in infiltration of monocytes and neutrophils into the CNS at least two weeks after sepsis in a CCR2 independent manner. Cellular inflammation is accompanied by long-term expression of pro-inflammatory cytokine and chemokine genes, including TNFα and CCR2 ligands, in whole brain homogenates. Gene expression analysis of microglia revealed that while microglia do express anti-microbial genes and damage-associated molecular pattern molecules of the S100A family of genes at least 2 weeks after sepsis, they do not express the cytokines observed in whole brain homogenates. Our results indicate that in a naturalistic model of infection, sepsis results in long-term neuroinflammation, and that this sustained inflammation is likely due to interactions among multiple cell types, including resident microglia and peripherally derived myeloid cells.
Title[redir]:
No title found...
Description:
Survivors of sepsis often experience long-term cognitive and functional decline. Previous studies utilizing lipopolysaccharide injection and cecal ligation and puncture in rodent models of sepsis have demonstrated changes in depressive-like behavior and learning and memory after sepsis, as well as evidence of myeloid inflammation and cytokine expression in the brain, but the long-term course of neuroinflammation after sepsis remains unclear. Here, we utilize cecal ligation and puncture with greater than 80% survival as a model of sepsis. We found that sepsis survivor mice demonstrate deficits in extinction of conditioned fear, but no acquisition of fear conditioning, nearly two months after sepsis. These cognitive changes occur in the absence of neuronal loss or changes in synaptic density in the hippocampus. Sepsis also resulted in infiltration of monocytes and neutrophils into the CNS at least two weeks after sepsis in a CCR2 independent manner. Cellular inflammation is accompanied by long-term expression of pro-inflammatory cytokine and chemokine genes, including TNFα and CCR2 ligands, in whole brain homogenates. Gene expression analysis of microglia revealed that while microglia do express anti-microbial genes and damage-associated molecular pattern molecules of the S100A family of genes at least 2 weeks after sepsis, they do not express the cytokines observed in whole brain homogenates. Our results indicate that in a naturalistic model of infection, sepsis results in long-term neuroinflammation, and that this sustained inflammation is likely due to interactions among multiple cell types, including resident microglia and peripherally derived myeloid cells.
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Doi.org employs WORDPRESS.
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Keywords {🔍}
clp, article, view, google, scholar, sepsis, mice, brain, pmid, pubmedncbi, days, ccr, fig, monocytes, cells, expression, fear, response, cns, immunoreactivity, conditioning, cell, results, microglia, longterm, lps, sham, activation, igg, observed, increased, inflammation, cognitive, neuroinflammation, extinction, plos, microglial, sections, controls, staining, hippocampus, systemic, signaling, context, tone, myeloid, learning, model, animals, unoperated,
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health central nervous system global inflammatory response cookies plos plos medicine contributed reagents/materials/analysis tools avidin-biotin complex cd45hi/cd11b+/ly6c+/ly6g- cells tumor necrosis factor-alpha post-traumatic stress symptoms long-lasting myeloid inflammation post-traumatic stress disorder castro-faria-neto hc open access article mediating nf-kappab activity complex networks long-term cognitive impairment public library cd45mid/cd11b+ cells expressed experience long-term cognitive methamphetamine-induced drug dependence lipopolysaccharide-induced microglial activation demonstrated long-lasting morphologic nominal inter-section distance long-term cognitive decline single high-dose administration cd45mid/cd11b+/cd64+ cells cd11b+/cd45mid/cd64+ cells goat anti-mouse polyclonal prespecified post-hoc comparisons blood-brain barrier permeability avidin-biotin system long-lasting myeloid infiltration single-dose lps relates complex balance nigrostriatal dopamine system antibodies include anti-ccr2 long-term sepsis survivors sepsis-surviving rats induced accession number e-mtab-4180 mouse blood-brain barrier monocyte/macrophage chemokines ccl2 set long-term neuroinflammatory age-matched controls housed express anti-microbial genes unoperated age-matched controls fear conditioning paradigm activated microglia-induced deficits dopamine systems
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