Aging leads to prolonged duration of inflammation-induced depression-like behavior caused by Bacillus Calmette-Guérin

Kelley, Keith W.; O’Connor, Jason C.; Lawson, Marcus A.; Dantzer, Robert; Rodriguez-Zas, Sandra L.; McCusker, Robert H.

doi:10.1016/j.bbi.2013.02.003

Cited by 44 publications

(40 citation statements)

References 38 publications

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“…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). More importantly, pharmacological or genetic inhibition of IDO prevents the development of depressive-/anxiety-like behaviors and cognitive impairments (Barichello et al, 2013;Henry et al, 2009;O'Connor et al, 2009a;O'Connor et al, 2009b;O'Connor et al, 2009c;Salazar et al, 2012;Xie et al, 2014).…”

Section: Neuropsychiatric Effects Of Inflammation: Evidence and Mechamentioning

confidence: 61%

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Capuron

Lasselin

Castanon

2016

Neuropsychopharmacol

135

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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 Mechamentioning

confidence: 61%

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Capuron

Lasselin

Castanon

2016

Neuropsychopharmacol

135

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“…These results are in agreement with previous studies using a number of mice strains and genotypes where BCG-challenged mice exhibited a drop in weight during the first 2 days post-challenge followed by a weight gain (Moreau et al, 2008; O’Connor et al, 2009; Platt et al, 2013; Painsipp et al, 2013; Vijaya Kumar et al, 2014). The speed of recovery of body weight varies with study and strain and meanwhile in some studies body weight does not differ among BCG-treated and BCG0 mice by Day 6 (Pratt et al, 2013; Painsipp et al, 2013), in other studies weight recovery is detected after Day 7 (Moreau et al, 2008; Kelley et al, 2013; Vijaya Kumar et al, 2014). …”

Section: Resultsmentioning

confidence: 99%

“…Six studies reported associations between BCG-treatment and sickness and depression-like behaviors in mice (Moreau et al, 2008; O’Connor et al, 2009; Kelley et al, 2013; Painsipp et al, 2013; Platt et al, 2013; Vijaya Kumar et al, 2014). In these studies, behavioral indicators were analyzed separately.…”

Section: Introductionmentioning

confidence: 99%

Advancing the understanding of behaviors associated with Bacille Calmette Guérin infection using multivariate analysis

Rodriguez-Zas

Nixon

Lawson

et al. 2015

Brain, Behavior, and Immunity

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Behavioral indicators in the murine Bacille Calmette Guérin (BCG) model of inflammation have been studied individually; however, the variability of the behaviors across BCG levels and the mouse-to-mouse variation within BCG-treatment group are only partially understood. The objectives of this study were: 1) to gain a comprehensive understanding of sickness and depression-like behaviors in a BCG model of inflammation using multivariate approaches, and 2) to explore behavioral differences between BCG-treatment groups and among mice within group. Adult mice were challenged with either 0mg (saline), 5mg or 10mg of BCG (BCG-treatment groups: BCG0, BCG5, or BCG10, respectively) at Day 0 of the experiment. Sickness indicators included body weight changes between Day 0 and Day 2 and between Day 2 and Day 5, and horizontal locomotor activity and vertical activity (rearing) measured at Day 6. Depression-like indicators included duration of immobility in the forced swim test and in the tail suspension test at Day 6 and sucrose consumption in the sucrose preference test at Day 7. The simultaneous consideration of complementary sickness and depression-like indicators enabled a more precise characterization of behavioral changes associated with BCG-treatment and of mouse-to-mouse variation, relative to the analysis of indicators individually. Univariate and multivariate analyses confirmed differences between BCG-treatment groups in weight change early on the trial. Significant differences between BCG-treatment groups in depression-like behaviors were still measurable after Day 5. The potential for multivariate models to account for the correlation between behavioral indicators and to augment the analytical precision relative to univariate models was demonstrated both for sickness and for depression-like indicators. Unsupervised learning approaches revealed the complementary information provided by the sickness and depression-like indicators considered. Supervised learning approaches using cross-validation confirmed subtle differences between BCG-treatment groups and among mice within group identified by the consideration of sickness and depression-like indicators. These findings support the recommendation for multivariate and multidimensional analyses of sickness and depression-like indicators to augment the systemic understanding of the behavioral changes associated with infection.

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“…These include (a) major contextual changes and stressors (e.g., retirement, disability, role loss; Rosow, 1973); (b) the loss of loved ones (e.g., Bruce et al, 1990; Onrust & Cuijpers, 2006); and (c) increased incidence of inflammation-triggering injury and disease (Alexopoulos & Morimoto, 2011). Comparative studies have found that older animals show exaggerated and prolonged sickness behavior in response to infection (e.g., Huang et al, 2008; Kelley et al, 2013) and human studies have found upregulated inflammatory activity with aging (Bruunsgaard, Pedersen, & Pedersen, 2001)—the degree of which correlates with depression (Baune et al, 2012). …”

Section: Individual Gender and Cultural Differences In Interoceptionmentioning

confidence: 99%

Interoceptive dysfunction: Toward an integrated framework for understanding somatic and affective disturbance in depression.

Harshaw

2015

Psychological Bulletin

213

147

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Depression is characterized by disturbed sleep and eating, a variety of other, nonspecific somatic symptoms, and significant somatic comorbidities. Why there is such close association between cognitive and somatic dysfunction in depression is nonetheless poorly understood. An explosion of research in the area of interoception—the perception and interpretation of bodily signals—over the last decade nonetheless holds promise for illuminating what have until now been obscure links between the social, cognitive-affective, and somatic features of depression. This paper reviews rapidly accumulating evidence that both somatic signaling and interoception are frequently altered in depression. This includes comparative studies showing vagus-mediated effects on depression-like behaviors in rodent models as well as studies in humans indicating both dysfunction in the neural substrates for interoception (e.g., vagus, insula, anterior cingulate cortex) and reduced sensitivity to bodily stimuli in depression. An integrative framework for organizing and interpreting this evidence is put forward which incorporates (a) multiple potential pathways to interoceptive dysfunction; (b) interaction with individual, gender, and cultural differences in interoception; and (c) a developmental psychobiological systems perspective, emphasizing likely differential susceptibility to somatic and interoceptive dysfunction across the lifespan. Combined with current theory and evidence, it is suggested that core symptoms of depression (e.g., anhedonia, social deficits) may be products of disturbed interoceptive-exteroceptive integration. More research is nonetheless needed to fully elucidate the relationship between mind, body, and social context in depression.

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Aging leads to prolonged duration of inflammation-induced depression-like behavior caused by Bacillus Calmette-Guérin

Cited by 44 publications

References 38 publications

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Advancing the understanding of behaviors associated with Bacille Calmette Guérin infection using multivariate analysis

Interoceptive dysfunction: Toward an integrated framework for understanding somatic and affective disturbance in depression.

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