Peripheral endotoxin induces hypothalamic immunoreactive interleukin‐1β in the rat

Hillhouse, E. W.; Mosley, K.

doi:10.1111/j.1476-5381.1993.tb13567.x

Cited by 61 publications

(32 citation statements)

References 8 publications

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“…Likewise, LPS exposure in the absence of the chronic ethanol exposure did not affect this measure of anxiety-like behavior. As LPS is known to increase cytokines in brain (Grinevich et al, 2001;Hagan et al, 1993;Hillhouse and Mosley, 1993;Ilyin et al, 1998;Matalka et al, 2005;Munhoz et al, 2006;Obuchowicz et al, 2006;Quan et al, 1994;Zujovic et al, 2001), it was speculated that the ability of the repeated LPS exposure to Figure 5 Persistent effect of repeated IL-1b, TNFa, or LPS on withdrawal-induced anxiety following re-exposure to 5 days of chronic ethanol starting 16 days later. Subgroups of rats from Figures 2 and 3 were treated with an additional 5 days of ethanol diet (4.5%) 16 days after having been exposed earlier to the initial repeated LPS or to the cytokines TNFa or IL-1b.…”

Section: Discussionmentioning

confidence: 99%

“…As LPS increases cytokines in brain (Breder et al, 1994;Buttini et al, 1997;Hagan et al, 1993;Hillhouse and Mosley, 1993;Ilyin et al, 1998;Matalka et al, 2005;Quan et al, 1994), it was next determined if cytokines could indeed be responsible for the LPS/withdrawal protocol sensitization of withdrawal-induced anxiety. To test this possibility, the cytokines (IL-1b, CCL2 (MCP-1), and TNFa (100 ng)) or vehicle were given i.c.v.…”

Section: Effect Of Repeated Cytokine Administration Before 5-days Of mentioning

confidence: 99%

“…Because the stress/withdrawal protocol sensitized anxiety following withdrawal from a single re-exposure to 5 days of ethanol (Overstreet et al, 2002;Breese et al, 2004), experiments were conducted to determine if LPS (which is known to increase brain cytokinesFBreder et al, 1994; Buttini et al, 1997;Hagan et al, 1993;Hillhouse and Mosley, 1993;Ilyin et al, 1998;Matalka et al, 2005;Quan et al, 1994; unpublished data) administered repeatedly before a single ethanol diet exposure would produce a similar effect as stress to sensitize withdrawal-induced anxiety. In this report, new data demonstrate that these two systemic administrations of varying LPS doses at weekly intervals before a single 5-day exposure to ethanol diet sensitized withdrawal-induced anxiety.…”

Section: Introductionmentioning

confidence: 99%

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Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Breese

Knapp

Overstreet

et al. 2007

Neuropsychopharmacol

100

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Previous investigations demonstrated that repeated stresses before an ethanol exposure sensitize ethanol withdrawal-induced anxietylike behavior ('anxiety'). In addition to activating the hypothalamic-pituitary-adrenal axis, acute stress also elevates cytokines in brain. Initially, to test possible cytokine involvement in this stress/withdrawal protocol, cytokines were increased in brain with 2 weekly repeated lipopolysaccharide (LPS) administrations (1000 m/kg) (LPS/withdrawal protocol) or with twice weekly intracerebroventricular (i.c.v.) administrations of the cytokines IL-1b, CCL2 (MCP-1) or TNFa (cytokine/withdrawal protocol) before exposure and withdrawal from a 5-day cycle of chronic ethanol diet. Both protocols sensitized withdrawal-induced anxiety and confirm cytokine involvement in the sensitized anxiety response. Testing of various doses of LPS (16-1000 mg/kg) and TNFa (3-100 ng, i.c.v.) demonstrated the dose-related nature of these protocols to sensitize withdrawal-induced anxiety. The sensitized anxiety was not produced by a single 5-day ethanol diet cycle or by repeated LPS or cytokine treatments alone. Likewise, sensitized anxiety in these protocols could not be attributed to differences in ethanol ingestion. When challenged with a subsequent re-exposure to a 5-day ethanol diet cycle 16 days after completion of the LPS/withdrawal or cytokine/withdrawal protocols, an increase in withdrawal-induced anxiety was observedFan indication of induction of an underlying persistent adaptive change. Finally, just as found previously with the stress/withdrawal protocol, administration of the benzodiazepine receptor antagonist flumazenil before the LPS or TNF treatments prevented anxiety sensitization. Together, these findings indicate that increased cytokine activity induces adaptive change that supports sensitization of ethanol withdrawal-induced anxiety that may be linked to GABA A -receptor function.

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Section: Discussionmentioning

confidence: 99%

Section: Effect Of Repeated Cytokine Administration Before 5-days Of mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Breese

Knapp

Overstreet

et al. 2007

Neuropsychopharmacol

100

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“…Indeed, various studies have consistently detected IL-1 in the CNS after brain injury or peripheral immune activation. For example, IL-1 bioactivity [8][9][10] , immunoreactivity [11][12][13] , mRNA [14][15][16] , and protein [17] have been shown to be present in brain after peripheral administration of lipopolysaccharide (LPS). Apart from its role in orchestrating inflammatory and host defense responses, IL-1 has also been implicated in learning and memory.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-1β with learning and memory

Huang

Sheng²

2010

Neurosci. Bull.

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Abstract:Interleukin-1 (IL-1) is one of the first cytokines ever described. It has long been recognized to play an important role in mediating inflammation and orchestrating the physiological and behavioral adjustments that occur during sickness.Recently, accumulating evidence has indicated that IL-1 also adversely affects cognitive function. Nevertheless, there are also some reports showing no effects or even beneficial effects of IL-1 on learning and memory. The relationship between IL-1 and cognitive impairment has not been clearly elucidated. Here we reviewed the evidence of both negative and positive effects of IL-1 on learning and memory, and the key factors that may affect the effects of IL-1 on learning and memory were discussed.

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“…Thus, administration of endotoxin has been reported to induce an increased cytokine expression in adult rat brains (7)(8)(9). In particular, a rise in the release of tumor necrosis factor-␣ (TNF-␣) has been thought to be associated with neuronal cell damage (10).…”

mentioning

confidence: 99%

Intracisternal Application of Endotoxin Enhances the Susceptibility to Subsequent Hypoxic-Ischemic Brain Damage in Neonatal Rats

Coumans

Middelanis²,

Garnier³

et al. 2003

Pediatr Res

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Perinatal brain damage is associated not only with hypoxicischemic insults but also with intrauterine inflammation. A combination of antenatal inflammation and asphyxia increases the risk of cerebral palsy Ͼ70 times. The aim of the present study was to determine the effect of intracisternal (i.c.) administration of endotoxin [lipopolysaccharides (LPS)] on subsequent hypoxic-ischemic brain damage in neonatal rats. Seven-day-old Wistar rats were subjected to i.c. application of NaCl or LPS (5 g/pup). One hour later, the left common carotid artery was exposed through a midline neck incision and ligated with 6-0 surgical silk. After another hour of recovery, the pups were subjected to a hypoxic gas mixture (8% oxygen/92% nitrogen) for 60 min. The animals were randomized to four experimental groups: 1) sham control group, left common carotid artery exposed but not ligated (n ϭ 5); 2) LPS group, subjected to i.c. application of LPS (n ϭ 7); 3) hypoxic-ischemic study group, i.c. injection of NaCl and exposure to hypoxia after ligation of the left carotid artery (n ϭ 17); or 4) hypoxic-ischemic/LPS study group, i.c. injection of LPS and exposure to hypoxia after ligation of the left carotid artery (n ϭ 19). Seven days later, neonatal brains were assessed for neuronal cell damage. In a second set of experiments, rat pups received an i.c. injection of LPS (5 g/pup) and were evaluated for tumor necrosis factor-␣ expression by immunohistochemistry. Neuronal cell damage could not be observed in the sham control or in the LPS group. In the hypoxicischemic/LPS group, neuronal injury in the cerebral cortex was significantly higher than in animals that were subjected to hypoxia/ischemia after i.c. application of NaCl. Injecting LPS intracisternally caused a marked expression of tumor necrosis factor-␣ in the leptomeninges. Applying LPS intracisternally sensitizes the immature rat brain to a subsequent hypoxicischemic insult. Hypoxic-ischemic cerebral damage is an important contributor to perinatal mortality and morbidity, including long-term neurologic sequelae in term and preterm fetuses (1, 2). However, as shown in recent studies, perinatal brain injury may be associated not only with hypoxic-ischemic insults but also with an ascending intrauterine inflammation before or during birth (3). It is widely known that Gram-negative anaerobic bacteria are involved in colonization and infection of the genitourinary tract in pregnant women, which could affect labor and preterm birth. Because pregnant women with fever and bacteriuria give birth to infants with a higher incidence of neurologic defects at 1 y of age than do mothers who are free of urinary tract infection (4), it seems that human maternal endotoxemia is associated with fetal CNS damage. Furthermore, there is a growing body of evidence from epidemiologic studies that exposure to placental inflammation before or during birth is accompanied by cerebral white matter damage, especially in the very preterm fetuses, i.e. those born before 32 wk of gestation (3). In addition, the ...

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Peripheral endotoxin induces hypothalamic immunoreactive interleukin‐1β in the rat

Cited by 61 publications

References 8 publications

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Interleukin-1β with learning and memory

Intracisternal Application of Endotoxin Enhances the Susceptibility to Subsequent Hypoxic-Ischemic Brain Damage in Neonatal Rats

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