Acute phase proteins in major depression

Berk, Michael; Wadee, Ahmed A.; Kuschke, Reverie H.; O’Neill-Kerr, Alex

doi:10.1016/s0022-3999(97)00139-6

Cited by 193 publications

(81 citation statements)

References 24 publications

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“…For instance, it is known that IL-6 is able to cross from the maternal circulation to the fetus in midgestation (Dahlgren et al, 2006), and that IL-6 derived from maternal circulation causes deficits in the behavioral response of adult mice to cope with stress (Smith et al, 2007) and decreases learning in adult rats . Interestingly, human patients diagnosed with depression have been shown to have serum IL-6 concentrations that are 10 times greater than those of control patients (Berk et al, 1997). It would be interesting to determine if the affective state of livestock or chronic exposures to stress could be regulating responses through cytokine modulation.…”

Section: Discussionmentioning

confidence: 99%

Effect of prenatal stress on subsequent response to mixing stress and a lipopolysaccharide challenge in pigs1

Lay

Kattesh

Cunnick

et al. 2011

Journal of Animal Science

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Sows subjected to prenatal stress have been found to produce offspring that have altered responses to stress. Our objective was to determine if exposing a sow to stress would alter the response of the offspring to lipopolysaccharide (LPS) at 2 mo of age or their response to mixing stress at 4 mo of age. Sow treatments consisted of intravenous injections of ACTH (1 IU/kg of BW), exposure to rough handling for a 10-min duration (rough), or no treatment (control) once per week from d 42 to 77 of gestation. At 2 mo of age, pigs from each treatment, 1 per litter (n = 21, 17, and 15 for the ACTH, rough, and control treatments, respectively), were challenged with 2 μg of LPS/kg of BW or saline, or served as a noninjected control. Their behavioral response to a human approach test and salivary cortisol were measured. At 4 mo of age, 1 pig from each treatment (n = 14, 14, and 15 for the ACTH, rough, and control treatments, respectively) was taken from its home pen and placed in a pen of unfamiliar pigs. At this time, a punch biopsy wound (6 × 6 mm) was created to measure the ability of the pig to heal the wound. At this same time, each pig received a 1-mL intramuscular injection of 20% ovine red blood cells (oRBC), and then a second injection of oRBC at 21 d postmixing. Blood samples were collected 3 times per week for 2 wk and then once a week for 4 more weeks. Blood samples were analyzed for cortisol, porcine corticosteroid-binding globulin, antibody response to oRBC, and nitric oxide production by macrophages. Behavior was recorded during the first 5 d after mixing. All pigs in the LPS challenge responded with characteristic sickness behavior; however, pigs in the rough treatment showed less sickness behavior than those in the other 2 treatments (P < 0.05). Maternal stress treatment did not affect (P < 0.43) salivary cortisol. Pigs from all treatments responded similarly to mixing stress with regard to cortisol, porcine corticosteroid-binding globulin, antibody titers, nitric oxide production, and hematology measures, and all pigs experienced the same amount of aggression in response to mixing. Without altering peripheral measures of stress responsivity, prenatal stress enhanced the ability of pigs to cope with a simulated immune challenge, which could prove to be an adaptation to challenging environments.

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Section: Discussionmentioning

confidence: 99%

Effect of prenatal stress on subsequent response to mixing stress and a lipopolysaccharide challenge in pigs1

Lay

Kattesh

Cunnick

et al. 2011

Journal of Animal Science

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“…The MCP-1, CD40L, and CRP biomarkers have also been studied, though to a lesser degree (Berk et al 1997;Danner et al 2003;Suarez et al 2003;Leo et al 2006). Previous studies on the relative abilities of non-SSRI, NRI, or SNRI, antidepressants (of which venlafaxine is an example) to down-regulate cytokines in depression have also been unclear (Kenis and Maes 2002;Tuglu et al 2003;Kubera et al 2004;Basterzi et al 2005;Lee and Kim 2006;Rybakowski et al 2006;Marques-Deak et al 2007).…”

Section: Discussionmentioning

confidence: 99%

“…For instance, high CRP in CAD patients is often considered a biomarker of acute plaque instability (Inoue et al 2005). Several earlier studies have reported elevations in MCP-1, CD40L, and CRP in depression (Berk et al 1997;Suarez et al 2003;Danner et al 2003;Leo et al 2006); however, no single study has examined all three of these markers in conjunction with such classic pro-inflammatory cytokines as TNFa and IL1b. Thus, in cases of ''medically healthy'' MDD patients, it is contended an elevation in any of these biomarkers may be an early warning of cardiovascular pathology (Anda et al 1993;Pratt et al 1996;Déchanet et al 1997;Lett et al 2004;Kamphuis et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Pro-inflammatory biomakers in depression: Treatment with venlafaxine

Piletz

Halaris²,

Iqbal³

et al. 2009

The World Journal of Biological Psychiatry

120

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High levels of pro-inflammatory biomarkers have been reported in depression. In the present study, five pro-inflammatory biomarkers were measured in the blood of patients with major depressive disorder (MDD). Biomarker levels were compared to age- and sex-matched healthy subjects. Patients with MDD had significantly higher baseline levels of tumour necrosis factor-alpha (TNFalpha, P=0.04), interleukin-1beta (IL1beta, P=0.03), and monocyte chemotactic protein-1 (MCP-1; P=0.02) compared to controls. There were no differences between groups in levels of cell determinant-40 ligand (CD40L) and C-reactive protein (CRP). A subset of the MDD patients consented to undergo treatment with venlafaxine (an SNRI: at lower doses a selective serotonin reuptake inhibitor; at higher doses also a norepinephrine reuptake inhibitor) for 8 weeks. By week 8, all treatment completers had responded therapeutically. However, levels of TNFalpha, IL1beta, and MCP-1 remained elevated. A concave quadratic equation described the associations between plasma venlafaxine concentrations and IL1beta (P=0.03), TNFalpha (P=0.09), and MCP-1 (P=0.02), suggesting that these biomarkers may have become selectively lowered in the serotonergic dose range of venlafaxine. This is the first report of venlafaxine's possible effect on pro-inflammatory biomarkers.

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“…To date, immune function in individuals with major depressive disorder (MDD) has been investigated by assessing levels of pro-inflammatory and acute-phase proteins [14]. Studies have shown that levels of interleukin (IL)-6 and C-reactive protein (CRP), and the immunologic complement component 4 (C4), but not C3, are significantly raised in patients with depression compared with controls [14].…”

Section: Inflammation and Redox Dysregulation In Mood Disordersmentioning

confidence: 99%

Aspirin: a review of its neurobiological properties and therapeutic potential for mental illness

Berk

Dean

Drexhage

et al. 2013

BMC Med

175

105

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There is compelling evidence to support an aetiological role for inflammation, oxidative and nitrosative stress (O&NS), and mitochondrial dysfunction in the pathophysiology of major neuropsychiatric disorders, including depression, schizophrenia, bipolar disorder, and Alzheimer's disease (AD). These may represent new pathways for therapy. Aspirin is a non-steroidal anti-inflammatory drug that is an irreversible inhibitor of both cyclooxygenase (COX)-1 and COX-2, It stimulates endogenous production of anti-inflammatory regulatory 'braking signals', including lipoxins, which dampen the inflammatory response and reduce levels of inflammatory biomarkers, including C-reactive protein, tumor necrosis factor-α and interleukin (IL)--6, but not negative immunoregulatory cytokines, such as IL-4 and IL-10. Aspirin can reduce oxidative stress and protect against oxidative damage. Early evidence suggests there are beneficial effects of aspirin in preclinical and clinical studies in mood disorders and schizophrenia, and epidemiological data suggests that high-dose aspirin is associated with a reduced risk of AD. Aspirin, one of the oldest agents in medicine, is a potential new therapy for a range of neuropsychiatric disorders, and may provide proof-of-principle support for the role of inflammation and O&NS in the pathophysiology of this diverse group of disorders.

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Acute phase proteins in major depression

Cited by 193 publications

References 24 publications

Effect of prenatal stress on subsequent response to mixing stress and a lipopolysaccharide challenge in pigs1

Effect of prenatal stress on subsequent response to mixing stress and a lipopolysaccharide challenge in pigs1

Pro-inflammatory biomakers in depression: Treatment with venlafaxine

Aspirin: a review of its neurobiological properties and therapeutic potential for mental illness

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