A new animal model of (chronic) depression induced by repeated and intermittent lipopolysaccharide administration for 4months

Kubera, Marta; Curzytek, Katarzyna; Duda, Weronika; Leśkiewicz, Monika; Basta‐Kaim, Agnieszka; Budziszewska, Bogusława; Román, Ádám; Zajı́cová, Alena; Holáň, Vladimı́r; Szczęsny, Ewa; Lasoń, W.; Maes, Michaël

doi:10.1016/j.bbi.2013.01.001

Cited by 97 publications

(68 citation statements)

References 59 publications

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“…In parallel with the lack of treatment effect on behaviour, we did not detect any differences in pro-inflammatory cytokines in the brain, such as IL-1β and IFN-γ, which are involved in inflammation-induced behavioural changes related to depression (19). In contrast, other studies showed that chronic LPS administration induced depressivelike behaviour (13,14). However, several differences in experimental design between these studies and ours, could explain this discrepancy.…”

Section: Discussioncontrasting

confidence: 70%

Chronic lipopolysaccharide infusion fails to induce depressive-like behaviour in adult male rats

Fischer

Liebenberg

Madsen

et al. 2015

Acta Neuropsychiatr.

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Section: Discussioncontrasting

confidence: 70%

Chronic lipopolysaccharide infusion fails to induce depressive-like behaviour in adult male rats

Fischer

Liebenberg

Madsen

et al. 2015

Acta Neuropsychiatr.

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“…Interestingly, animal depression models based on psychosocial stress show that depression-like behaviors are associated with activated immune-inflammatory and oxidative and nitrosative stress (O&NS) pathways [24,25]. New animal models of depression have been developed based on chronic (repeated intermittent) administration of LPS and peripheral and central activation of the TLR complex and [26][27][28]. The latter studies suggest a bifunctional role of TLR-4 signaling pathway by triggering neuroinflammation at prefrontal cortex level and by regulating gut barrier function and permeability [27,28].…”

Section: Inflammation Is Not the Only Drug Target In Depressionmentioning

confidence: 99%

Toward Omics-Based, Systems Biomedicine, and Path and Drug Discovery Methodologies for Depression-Inflammation Research

et al. 2015

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Meta-analyses confirm that depression is accompanied by signs of inflammation including increased levels of acute phase proteins, e.g. C-reactive protein, and pro-inflammatory cytokines, e.g. interleukin-6. Supporting the translational significance of this, a meta-analysis showed that anti-inflammatory drugs may have antidepressant effects. Here we argue that inflammation and depression research needs to get onto a new track. Firstly, the choice of inflammatory biomarkers in depression research was often too selective and did not consider the broader pathways.Secondly, although mild inflammatory responses are present in depression, other immune-related pathways cannot be disregarded as new drug targets, e.g. activation of cell-mediated immunity, oxidative and nitrosative stress (O&NS) pathways, autoimmune responses, bacterial translocation, activation of the Toll-like Receptor and neuroprogressive pathways. Thirdly, antiinflammatory treatments are sometimes used without full understanding of their effects on the broader pathways underpinning depression. Since many of the activated immune-inflammatory pathways in depression actually confer protection against an overzealous inflammatory response, targeting these pathways may result in unpredictable and unwanted results. Furthermore, this paper discusses the required improvements in research strategy, i.e. path and drug discovery processes, omics-based techniques and systems biomedicine methodologies. Firstly, novel methods should be employed to examine the intracellular networks that control and modulate the immune, O&NS and neuroprogressive pathways using omics-based assays, including genomics, transcriptomics, proteomics, metabolomics, epigenomics and microbiomics. Secondly, systems biomedicine analyses are essential to unravel the complex interactions between these cellular 4 networks, pathways and the multifactorial trigger factors and to delineate new drug targets in the cellular networks or pathways. Drug discovery processes should delineate new drugs targeting the intracellular networks and immune-related pathways.

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“…LPS-induced depressed behavior has been used to investigate the inflammatory mechanisms involved in mood disorders (Dantzer et al, 2008;Kubera et al, 2013;Maes et al, 2012). The depressive-like and sickness behaviors emerge as a physiological response to combat infections and protect the organism.…”

mentioning

confidence: 99%

“…LPS-induced sickness and depression-like behavior has been used as a model of clinical depression (Dantzer et al, 2008;Kubera et al, 2013;Maes et al, 2012).…”

mentioning

confidence: 99%

Cocaine counteracts LPS-induced hypolocomotion and triggers locomotor sensitization expression

Tortorelli

Engelke

Lunardi

et al. 2015

Behavioural Brain Research

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A new animal model of (chronic) depression induced by repeated and intermittent lipopolysaccharide administration for 4months

Cited by 97 publications

References 59 publications

Chronic lipopolysaccharide infusion fails to induce depressive-like behaviour in adult male rats

Chronic lipopolysaccharide infusion fails to induce depressive-like behaviour in adult male rats

Toward Omics-Based, Systems Biomedicine, and Path and Drug Discovery Methodologies for Depression-Inflammation Research

Cocaine counteracts LPS-induced hypolocomotion and triggers locomotor sensitization expression

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