2004
DOI: 10.1016/j.physbeh.2004.08.030
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A profile of the immediate endocrine, metabolic and behavioural responses following a dual exposure to endotoxin in early life

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Cited by 32 publications
(24 citation statements)
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“…Beyond the obvious difference that LPS is not a replicating pathogen, one striking difference between the LPS model and E. coli infection is the pattern of corticosterone production following the challenge: LPS results in a dramatic increase in corticosterone (4 fold or more) the first day of challenge (P3), but virtually complete resistance to subsequent challenge on P5 (Walker et al, 2004a;2004b). Following E. coli infection, concentrations increase 2-3 fold and remain elevated for at least 48 h (Bilbo et al, 2005a).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Beyond the obvious difference that LPS is not a replicating pathogen, one striking difference between the LPS model and E. coli infection is the pattern of corticosterone production following the challenge: LPS results in a dramatic increase in corticosterone (4 fold or more) the first day of challenge (P3), but virtually complete resistance to subsequent challenge on P5 (Walker et al, 2004a;2004b). Following E. coli infection, concentrations increase 2-3 fold and remain elevated for at least 48 h (Bilbo et al, 2005a).…”
Section: Discussionmentioning
confidence: 99%
“…Unfortunately, there are no data, to our knowledge, on depressive-like behavior in adulthood following neonatal LPS. Interestingly, there are reports that P3/P5 LPS increases anxiety-like behavior in adulthood (Breivik et al, 2002;Walker et al, 2004a), which is often associated with depression. In contrast, Spencer et al (2006) report no significant change in adult anxiety following LPS on P7.…”
Section: Discussionmentioning
confidence: 99%
“…In adulthood, this increase in glucocorticoids is associated with an increased basal and stress-induced glucocorticoid release [6], which is correlated with a decrease in IL-1 production. These findings indicate that glucocorticoid exposure during fetal life tends to promote a TH2 immunophenotype that is associated with decreased pro-inflammatory, but increased allergic responses to stimulation in later life.…”
Section: Hpa-axis Programming and Immunitymentioning
confidence: 99%
“…A number of studies have shown that the hormonal and metabolic environment during perinatal life can have a profound and persistent influence on outcomes related to body composition, metabolic activity [4], neuroendocrine [5] and immune functioning [6,7], as well as nociceptive sensitivity [8]. The mechanism proposed to be central to these negative health consequences is programming of the HPA axis.…”
Section: Mechanisms Underlying Fetal Programming Of the Hpa Axismentioning
confidence: 99%
“…Early immune challenge has emerged as a model of early-life adversity with a distinct focus on the impact of immune activation during CNS development on stress-related phenotypes [7] . Postnatal challenge with lipopolysaccharide (LPS), a cell wall constituent of gram-negative bacteria, during the first week of life (postnatal day (P)3 and 5) enhances the adult neuroendocrine and behavioral response to stress [8,9] and increases basal or stress-induced anxiety-related behaviors [10] . Male and female rodents have different susceptibility to the acute [4] and long-term consequences of LPS challenge [3,11] with a recent study demonstrating clear differences in anxiety-related behaviors of adult male and female LPS-challenged rats [12] .…”
Section: Research Articlementioning
confidence: 99%