Schizophrenia and Immune Responses

Gaughran, Fiona; Welch, J

doi:10.1007/978-0-387-30398-7_21

Cited by 4 publications

(7 citation statements)

References 171 publications

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“…On the other hand, expression levels of IL6 mRNA were significantly decreased in male MIA-ACE offspring during adolescence but not adulthood. Increased levels of IL6 are found in schizophrenia, with levels highest in individuals experiencing acute episodes and associated with longer duration of illness and treatment resistance ( Gaughran and Welch, 2008 ). Furthermore, IL6 is demonstrated to reduce interstitial dopamine levels and to modulate the serotonin response in the rat hypothalamus ( Gaughran and Welch, 2008 ).…”

Section: Discussionmentioning

confidence: 99%

“…Increased levels of IL6 are found in schizophrenia, with levels highest in individuals experiencing acute episodes and associated with longer duration of illness and treatment resistance ( Gaughran and Welch, 2008 ). Furthermore, IL6 is demonstrated to reduce interstitial dopamine levels and to modulate the serotonin response in the rat hypothalamus ( Gaughran and Welch, 2008 ). In support of our findings, we have previously shown in the rat that a combination of MIA and ACE can induce abnormal elevation of serotonin 5HT 1A receptor binding in the hippocampus of late adolescent, young adult and adult offspring ( Dalton et al., 2012 ).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, there is evidence that the hypothalamic-pituitary-adrenal (HPA) axis, a vital component of the GBA, is dysregulated in patients with schizophrenia. This dysregulation is thought to be mediated by increased levels of proinflammatory cytokines such as interleukin 6 (IL6) ( Gaughran and Welch, 2008 ).…”

Section: Introductionmentioning

confidence: 99%

“…1 ). Evidence suggests that altered immune functioning may contribute to the aetiology and pathogenesis of schizophrenia, with patients exhibiting an inflammatory profile that correlates with symptom severity ( Bergink et al., 2014 ; Gaughran and Welch, 2008 ). In the present study, we examine the effect of combined environmental stressors on inflammation, the HPA axis, intestinal barrier and gut bacteria.…”

Section: Introductionmentioning

confidence: 99%

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Investigating the gut-brain axis in a neurodevelopmental rodent model of schizophrenia

Katz-Barber

Hollins

Cuskelly

et al. 2020

Brain, Behavior, & Immunity - Health

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Background Although the aetiology of schizophrenia remains unknown, it has been suggested that it might occur in response to alterations in the gut-brain axis (GBA), the bi-directional communication system between the gut and the brain. The current study aimed to determine whether the “two-hit” animal model of neuropsychopathology (maternal immune activation combined with adolescent cannabinoid exposure), produced abnormalities in the GBA Method Pregnant Wistar rats were administered the viral mimetic polyI:C on gestational day 19 and offspring were administered the synthetic cannabinoid HU210 from postnatal days 35–48. Evidence of GBA activation was assessed in the hypothalamus, colon and fecal samples from male and female offspring at adolescence and adulthood Results Findings were sex-specific with adolescent female offspring exhibiting an increased hypothalamic inflammatory profile, increased hypothalamic CRHR1 mRNA, and decreased fecal expression of Bifidobacterium longum , however, no changes were detected in colonic inflammation or integrity. Conclusion These results indicate that the rat two-hit model, documented to produce behavioural and neuroanatomical abnormalities, also produces hypothalamic and microbiota abnormalities. The results also demonstrate significant sex differences, suggesting that this model may be useful for investigating the role of the GBA in the aetiology of neurodevelopmental disorders such as schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Investigating the gut-brain axis in a neurodevelopmental rodent model of schizophrenia

Katz-Barber

Hollins

Cuskelly

et al. 2020

Brain, Behavior, & Immunity - Health

View full text Add to dashboard Cite

show abstract

“…Central nervous system Reduced brain volume and gray matter in various brain areas, both in chronic and early onset patients 31,32 Reduced brain weight and regionally distributed pattern of gray matter atrophy 37 Frontal cortex dysfunction (hypo-frontality), 33 fronto-temporal disconnectivity 34 Distinct prefrontal cortex regions exhibit different patterns of functional change 38 Neurocognitive deficits, including executive functioning, working memory, attention and episodic memory 35,36 Decline in short-term and episodic memory 39 Eyes Increased prevalence of cataracts, not fully attributed to medication 40 Increased opacities of the lens 41 Immune system, cytokines IL-1β, IL-6, IL-3, IL-4, IL-10, IL-13, TNF-α: increased serum levels IL-1, IL-6, IL-8, IL-10, IL-12, TNF-α: increased serum levels IL-2, INF-a, INF-γ: reduced serum levels 42,43 IL-2, INF-γ: reduced serum levels 44 Hormonal system Abnormalities in gonadal hormones and endocrine function:…”

Section: Schizophreniamentioning

confidence: 99%

Schizophrenia as segmental progeria

2011

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Schizophrenia is associated with a variety of physical manifestations (i.e. metabolic, neurological) and despite psychotropic medication being blamed for some of these (in particular obesity and diabetes), there is evidence that schizophrenia itself confers an increased risk of physical disease and early death. The observation that schizophrenia and progeroid syndromes share common clinical features and molecular profiles gives rise to the hypothesis that schizophrenia could be conceptualized as a whole body disorder, namely a segmental progeria. Mammalian cells employ the mechanisms of cellular senescence and apoptosis (programmed cell death) as a means to control inevitable DNA damage and cancer. Exacerbation of those processes is associated with accelerated ageing and schizophrenia and this warrants further investigation into possible underlying biological mechanisms, such as epigenetic control of the genome.

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Inflammation and viral infection as disease modifiers in schizophrenia

Klein,

Guest,

Dobrowolny

et al. 2023

Front. Psychiatry

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Numerous studies have now implicated a role for inflammation in schizophrenia. However, many aspects surrounding this aspect of the disease are still controversial. This controversy has been driven by conflicting evidence on the role of both pro-and anti-inflammatory factors and by often contentious findings concerning cytokine and immune cell profiles in the central nervous system and periphery. Current evidence supports the point that interleukin-6 is elevated in CSF, but does not support activation of microglia, resident macrophage-like cells in the brain. Furthermore, the mechanisms involving transit of the peripheral immune system factors across the blood brain barrier to central parenchyma have still not been completely elucidated. This process appears to involve perivascular macrophages and accompanying dendritic cells retained in the parenchyma by the chemokine and cytokine composition of the surrounding milieu. In addition, a number of studies have shown that this can be modulated by infection with viruses such as herpes simplex virus type I which may disrupt antigen presentation in the perivascular space, with long-lasting consequences. In this review article, we discuss the role of inflammation and viral infection as potential disease modifiers in schizophrenia. The primary viral hit may occur in the fetus in utero, transforming the immune response regulatory T-cells or the virus may secondarily remain latent in immune cells or neurons and modify further immune responses in the developing individual. It is hoped that unraveling this pathway further and solidifying our understanding of the pathophysiological mechanisms involved will pave the way for future studies aimed at identification and implementation of new biomarkers and drug targets. This may facilitate the development of more effective personalized therapies for individuals suffering with schizophrenia.

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Schizophrenia and Immune Responses

Cited by 4 publications

References 171 publications

Investigating the gut-brain axis in a neurodevelopmental rodent model of schizophrenia

Investigating the gut-brain axis in a neurodevelopmental rodent model of schizophrenia

Schizophrenia as segmental progeria

Inflammation and viral infection as disease modifiers in schizophrenia

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