2016
DOI: 10.1016/j.bbi.2016.06.007
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Diet-induced obesity prolongs neuroinflammation and recruits CCR2 + monocytes to the brain following herpes simplex virus (HSV)-1 latency in mice

Abstract: Herpes simplex virus (HSV)-1 is a ubiquitous human infection, with increased prevalence in obese populations. Obesity has been linked to increased inflammation, susceptibility to infection, and higher rates of anxiety disorder and cognitive impairment. To determine how obesity alters neuroinflammation and behavior following infection, we infected weanling C57BL/6 or CCR2RFP/+/CX3CR1GFP/+ mice with a very low dose of HSV-1. Following viral latency (14 days post infection (d p.i.)), mice were randomly assigned t… Show more

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Cited by 10 publications
(9 citation statements)
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“…Indeed, macrophages clear viral particles and apoptotic cells, release pro-inflammatory cytokines and chemokines to attract additional innate immune cells, limit viral replication, process, and present viral antigens to lymphocytes (Kodukula et al, 1999 ). Quite the opposite, infiltrating macrophages producing pro-inflammatory cytokines have been described also during latent HSV-1 infection and correlate with prolonged neuroinflammation in hypothalamus and hippocampus (White et al, 2016 ). Indeed, during chronic HSV-1 infection recruited immune cells impact the integrity of peripheral nerves either directly by damaging neurons harboring the virus or through the secretion of soluble factors that modify gene expression and survival of infected and non-infected cells (Kramer et al, 2003 ; Dosa et al, 2011 ).…”
Section: Introductionmentioning
confidence: 99%
“…Indeed, macrophages clear viral particles and apoptotic cells, release pro-inflammatory cytokines and chemokines to attract additional innate immune cells, limit viral replication, process, and present viral antigens to lymphocytes (Kodukula et al, 1999 ). Quite the opposite, infiltrating macrophages producing pro-inflammatory cytokines have been described also during latent HSV-1 infection and correlate with prolonged neuroinflammation in hypothalamus and hippocampus (White et al, 2016 ). Indeed, during chronic HSV-1 infection recruited immune cells impact the integrity of peripheral nerves either directly by damaging neurons harboring the virus or through the secretion of soluble factors that modify gene expression and survival of infected and non-infected cells (Kramer et al, 2003 ; Dosa et al, 2011 ).…”
Section: Introductionmentioning
confidence: 99%
“…However, others failed to reproduce this hippocampal microglial activation by an obesogenic diet, reporting no differences in the microglial process length, Iba-1+ immunoreactivity and/or cell number [ 41 , 59 , 60 ]. One group even observed a decrease in the Iba-1+ area fraction in hippocampi from rats fed a hypercaloric diet, compared to control animals [ 61 ].…”
Section: Hippocampusmentioning
confidence: 99%
“…Obesity caused robust DG microglial activation with increased microglial cell numbers in the hilar region when compared to controls [ 59 , 65 , 69 ]. This microglial activation persisted in the molecular and granule dentate cell layers when animals were chronically exposed to an obesogenic diet.…”
Section: Hippocampusmentioning
confidence: 99%
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“…Recruitment of macrophages and lymphocytes nearby infected neurons or glial cells represents a key step to limit replication and spread of neurotropic viruses. However, the inflammatory infiltrate potentially damages the neuronal tissue through direct or indirect mechanisms ( Kodukula et al, 1999 ; White et al, 2016 ).…”
Section: Introductionmentioning
confidence: 99%