Poly I:C-induced activation of the immune response is accompanied by depression and anxiety-like behaviours, kynurenine pathway activation and reduced BDNF expression

Gibney, Sinead M.; McGuinness, B. W.; Prendergast, Catriona T.; Harkin, Andrew; Connor, Thomas J.

doi:10.1016/j.bbi.2012.11.010

Cited by 197 publications

(168 citation statements)

References 93 publications

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“…In support of this notion, brain or cerebrospinal fluid concentrations of kynurenine neurotoxic metabolites are elevated in several neuropsychiatric or neurodegenerative diseases (Campbell et al, 2014;Schwarcz et al, 2001;Steiner et al, 2011;Stone et al, 2012) and have been related to the stretch of brain damages, impaired neurogenesis, and development of neuropsychiatric symptoms (Savitz et al, 2015a;Savitz et al, 2015b;Stone et al, 2012;Zunszain et al, 2012). In line with clinical findings, preclinical studies performed in rodents treated with an immune challenge have documented associations between emotional/cognitive alterations and both peripheral and brain IDO activation (Andre et al, 2008;Corona et al, 2013;Frenois et al, 2007;Gibney et al, 2013;Lawson et al, 2013;Lestage et al, 2002;Moreau et al, 2005Moreau et al, , 2008Salazar et al, 2012;Xie et al, 2014). In addition, aged mice or mice with constitutive microglial overactivation display, upon immune challenge, sustained cytokine production together with protracted brain IDO expression and depressive-like behavior (Corona et al, 2010;Godbout et al, 2008;Kelley et al, 2013).…”

Section: Neuropsychiatric Effects Of Inflammation: Evidence and Mechasupporting

confidence: 53%

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Capuron

Lasselin

Castanon

2016

Neuropsychopharmacol

141

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Depression and metabolic disorders, including overweight and obesity, appear tightly interrelated. The prevalence of these conditions is concurrently growing worldwide, and both depression and overweight/obesity represent substantial risk factors for multiple medical complications. Moreover, there is now multiple evidence for a bidirectional relationship between depression and increased adiposity, with overweight/obesity being associated with an increased prevalence of depression, and in turn, depression augmenting the risk of weight gain and obesity. Although the reasons for this intricate link between depression and increased adiposity remain unclear, converging clinical and preclinical evidence points to a critical role for inflammatory processes and related alterations of brain functions. In support of this notion, increased adiposity leads to a chronic low-grade activation of inflammatory processes, which have been shown elsewhere to have a potent role in the pathophysiology of depression. It is therefore highly possible that adiposity-driven inflammation contributes to the development of depressive disorders and their growing prevalence worldwide. This review will present recent evidence in support of this hypothesis and will discuss the underlying mechanisms and potential therapeutic targets. Altogether, findings presented here should help to better understand the mechanisms linking adiposity to depression and facilitate the identification of new preventive and/or therapeutic strategies.

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Section: Neuropsychiatric Effects Of Inflammation: Evidence and Mechasupporting

confidence: 53%

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Capuron

Lasselin

Castanon

2016

Neuropsychopharmacol

141

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“…While the dose of poly I:C used in this study was higher than that used in our previous study [45], it is similar to that used in other studies with conventional mice or rats which produce altricial offspring. This poly I:C dose (5 mg/kg) had no effect on the duration of pregnancy, litter size and neonatal survival; however, unlike that used in our previous study, this higher dose of poly I:C did cause an acute decrease in maternal body weight, an indicator of sickness behaviour used in previous studies [66]. As prenatal poly I:C administration caused a decrease in postnatal growth, although not significantly, it is important to consider whether this higher dose of poly I:C may have caused a global compromise and, if so, what effect this may have had on postnatal behaviour.…”

Section: Discussioncontrasting

confidence: 39%

Prenatal Exposure to the Viral Mimetic Poly I:C Alters Fetal Brain Cytokine Expression and Postnatal Behaviour

et al. 2014

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An increased incidence of mental illness disorders is found in children and adolescents born to mothers who experienced an infection-based illness during pregnancy. Animal models to study the prenatal origin of such outcomes of pregnancy have largely used conventional rodents, which are immature (altricial) at birth compared with the human neonate. In this study, we used the precocial spiny mouse (Acomys cahirinus), whose offspring have completed organogenesis at birth, and administered a single subcutaneous injection of a 5 mg/kg dose of the viral mimetic poly I:C (polyriboinosinic-polyribocytidylic acid) at mid gestation (20 days; term is 39 days). Prenatal exposure to poly I:C caused a transient weight loss in the pregnant dam, produced a downregulation of the proinflammatory cytokine tumour necrosis factor-α in the fetal brain, and resulted in abnormalities in sensorimotor gating and reduced social interaction, memory and learning in juvenile offspring. No changes in exploratory activity or anxiety and fear behaviours were found between the treatment groups. This study provides evidence that, in a rodent model that more closely resembles human brain development, prenatal infection can lead to behavioural abnormalities in postnatal life.

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“…First, depressive-like behavior is common in animals subjected to inflammatory insults [37,38]. Second, mood disturbance is common after infection [39].…”

Section: The Contribution Of Inflammation To Depression and Fatiguementioning

confidence: 99%

“…The FAS has been validated in healthy cohorts [71]. FAS scores of 10-21 indicate that the patient is "not tired", scores of 22-34 indicate that the patient is "tired", and scores of [35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50] indicate that the patient is "very tired" [72]. We evaluated the relationship between the biomarkers of inflammation shown in Fig.…”

Section: Inflammation and The Biological Basis Of Psfmentioning

confidence: 99%

Inflammation and the Silent Sequelae of Stroke

Becker

2016

Neurotherapeutics

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Depression and fatigue are common after stroke and negatively impact the quality of life of stroke survivors. The biological bases of these symptoms are unknown, but an abundance of data point to a role for inflammation. This review highlights evidence supporting the contribution of inflammation to poststroke depression and poststroke fatigue. Potential treatments for poststroke depression and poststroke fatigue are explored, with a special emphasis on those that modulate the immune response.

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Poly I:C-induced activation of the immune response is accompanied by depression and anxiety-like behaviours, kynurenine pathway activation and reduced BDNF expression

Cited by 197 publications

References 93 publications

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Prenatal Exposure to the Viral Mimetic Poly I:C Alters Fetal Brain Cytokine Expression and Postnatal Behaviour

Inflammation and the Silent Sequelae of Stroke

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