New Insights into Cytokine Gene Expression in the Rat Hypothalamus Following Endotoxin Challenge

Jessop, David S.; Besedovsky, Hugo O.; Rey, Adriana del

doi:10.1007/s11064-009-0071-0

Cited by 3 publications

(2 citation statements)

References 32 publications

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“…Importantly, if male rats are infected with E. coli on postnatal day 30 (P30), well after the neonatal period of development, no alterations in inflammatory cytokine production or behavior are observed in adulthood in response to LPS (Bilbo et al, 2006). Taken together, these data suggest that the immune system is permanently altered or programmed by early life immune activation or inflammation (Del Rey et al, 2009;Jessop et al, 2010) and that the immune system and the molecules it produces (e.g. cytokines) are key mediators of the cognitive and behavioral impairments observed in adulthood.…”

Section: Introductionmentioning

confidence: 97%

Neonatal infection produces significant changes in immune function with no associated learning deficits in juvenile rats

Osborne

Caulfield

Solomotis

et al. 2017

Developmental Neurobiology

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The current experiments examined the impact of early-life immune activation and a subsequent mild immune challenge with lipopolysaccharide (LPS; 25μg/kg) on hippocampal-dependent learning, proinflammatory cytokine expression in the brain, and peripheral immune function in juvenile male and female rats at P24, an age when hippocampal-dependent learning and memory first emerges. Our results indicate that neonatal infection did not produce learning deficits in the hippocampal-dependent context pre-exposure facilitation effect paradigm in juvenile males and females, contrary to what has been observed in adults. Neonatal infection produced an increase in baseline IL-1b expression in the hippocampus (HP) and medial prefrontal cortex (mPFC) of juvenile rats. Furthermore, neonatally infected rats showed exaggerated IL-1β expression in the HP following LPS treatment as juveniles; and juvenile females, but not males, showed exaggerated IL-1β expression in the mPFC following LPS treatment. Neonatal infection attenuated the production of IL-6 expression following LPS treatment in both the brain and the spleen, and neonatal infection decreased the numbers of circulating white blood cells in juvenile males and females, an effect that was further exacerbated by subsequent LPS treatment. Together, our data indicate that the consequences of neonatal infection are detectable even early in juvenile development, though we found no concomitant hippocampal-dependent learning deficits at this young age. These findings underscore the need to consider age and associated on-going neurodevelopmental processes as important factors contributing to the emergence of cognitive and behavioral disorders linked to early-life immune activation.

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Section: Introductionmentioning

confidence: 97%

Neonatal infection produces significant changes in immune function with no associated learning deficits in juvenile rats

Osborne

Caulfield

Solomotis

et al. 2017

Developmental Neurobiology

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“…TLR4 appears to be a specific receptor for lipopolysaccharide (LPS), an integral component of the outer membrane of Gram negative bacteria [9,10]. LPS dramatically induces a production of many proinflammatory factors and their gene expressions [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Time-Course Alterations of Toll-Like Receptor 4 and NF-κB p65, and Their Co-Expression in the Gerbil Hippocampal CA1 Region After Transient Cerebral Ischemia

Yoo

Hwang

et al. 2011

Neurochem Res

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Innate immune system is very important to modulate the host defense against a large variety of pathogens. Toll-like receptors (TLRs) play a key role in controlling innate immune response. Among TLRs, TLR4 is a specific receptor for lipopolysaccharide and associated with the release of pro-inflammatory cytokines. In the present study, we investigated ischemia-related changes of TLR4 immunoreactivity and its protein level, and nuclear factor κB (NF-κB) p65 immunoreactivity regarding inflammatory responses in the hippocampal CA1 region after 5 min of transient cerebral ischemia to identify the correlation between transient ischemia and inflammation. In the sham-operated group, TLR4 immunoreactivity was easily detected in pyramidal neurons of the hippocampal CA1 region (CA1). TLR4 immunoreactivity in pyramidal neurons was distinctively decreased after ischemia/reperfusion (I/R); instead, based on double immunofluorescence study, TLR4 immunoreactivity was expressed in non-pyramidal neurons and astrocytes from 2 days postischemia. In addition, TLR4 protein level was lowest at 1 day postischemia and highest 4 days after I/R. On the other hand, NF-κB p65 immunoreactivity was not detected in the CA1 of the sham-operated group, and NF-κB p65 immunoreactivity was not observed until 1 day after I/R. However, NF-κB p65 immunoreactivity began to be expressed in astrocytes at 2 days postischemia, and the immunoreactivity was strong 4 days postischemia. Our results indicate that TLR4 and NF-κB p65 immunoreactivity are changed in CA1 pyramidal neurons and newly expressed in astrocytes, not in microglia, in the CA1 region after transient cerebral ischemia.

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Effect of inflammatory challenge on hypothalamic neurons expressing orexinergic and melanin-concentrating hormone

Palomba

Etet

Veronesi

2014

Neuroscience Letters

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New Insights into Cytokine Gene Expression in the Rat Hypothalamus Following Endotoxin Challenge

Cited by 3 publications

References 32 publications

Neonatal infection produces significant changes in immune function with no associated learning deficits in juvenile rats

Neonatal infection produces significant changes in immune function with no associated learning deficits in juvenile rats

Time-Course Alterations of Toll-Like Receptor 4 and NF-κB p65, and Their Co-Expression in the Gerbil Hippocampal CA1 Region After Transient Cerebral Ischemia

Effect of inflammatory challenge on hypothalamic neurons expressing orexinergic and melanin-concentrating hormone

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