Elevated interleukin-2, interleukin-6 and interleukin-8 serum levels in neuroleptic-free schizophrenia: association with psychopathology

Zhang, Xiang Yang; Zhou, Dong; Zhang, Pei Yan; Wu, Gui Ying; Cao, Lian Yuan; Shen, Yanying

doi:10.1016/s0920-9964(01)00296-1

Cited by 183 publications

(105 citation statements)

References 59 publications

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“…Zanimljivo je što su podaci često heterogeni kada je u pitanju posmatranje nivoa citokina u odnosu na kliničke varijable. Tako se povišene koncentracije IL-6 dovode u vezu sa negativnom fenomenologijom, dužinom bolesti, teraporezistencijom, nepovoljnim ishodom bolesti, akutnom fazom bolesti, ali i sa hronič-nim-rezidualnim formama shizofrenije [37][38][39][40][41]. Mali broj istraživanja se bavio razlikama u odnosu na "subgrupe" obolelih.…”

Section: Alteracije Citokina Zapažene Kod Obolelih Od Shizofrenije-klunclassified

Schizophrenia and cytokines

Dunjić-Kostić¹,

Pantović-Stefanović²,

Ivković³

et al. 2015

Engrami

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Razvoj sofisticiranih tehnika detekcije strukturnih i biohemijskih abnormlnosti, u poslednjih nekoliko decenija, odigrao je važnu ulogu u preciznijem sagledavanju brojnih bioloških alteracija kod pacijenata uopšte. Ova činjenica je od posebne važnosti istraživačima u oblasti neuronauka, zbog često nepoznate i/ili multifaktorijalne etiopatogeneze neuropsihijatrijskih poremećaja, te svaki deo spoznaje kompleksnog "algoritma" ima svoje značajno mesto. U poslednje vreme veliku pažnju istraživača privlače eksploracija imunoloških abnormalnosti kod obolelih od shizofrenije, kao i citokinima posredovani mehanizmi koji predstavljaju osnovu za niz hipoteza iznesenih na ovu temu [1][2][3]. U daljem tekstu fokusiraće-mo se na nekoliko najvažnijih teorijskih pravaca koje se tiču inflamacije i imunoloških promena zapaženih u shizofreniji. Jedna od teorija je da je infekcija majke tokom trudnoće (naročito tokom ranog perinatalnog perioda) značajan faktor rizika za dete za razvoj shizofrenije i drugih neurorazvojnih oboljenja [4,5]. Epidemiološke studije su pokazale da infekcija majke virusom influence tokom trudnoće povećava rizik za shizofreniju deteta za 3-7 puta [4,6]. Pored virusa influence i brojni drugi infektivni činioci su povezani sa povećanim rizikom za SCH medju kojima su i varicela zoster virus, polio, difterija, rubela itd [5]. Medjutim, patološki mehanizam odgovoran za povećan rizik za shizofreniju kod dece nakon izloženosti majke infekciji još uvek je nedovoljno jasan. Takodje otvoreno je pitanje, na koji način infekcija majke dovodi do citokinskog disbalansa kod fetusa; da li je u pitnju delovanje infektivnog činioca na specifične receptore koji dovode do produkcije i oslobadjanja različitih medijatora zapaljenja u periferni majčin imuni sistem koji onda prolaze placentu i ulaze u cirkulaciju fetusa [6,7], ili potencijalni iz- Kratak sadržajPoslednjih par decenija pažnju istraživača sve više privlače imunološke abnormalnosti uočene kod obolelih od shizofrenije. U prvom delu teksta prikazan je kratak pregled pojedinih teorijskih konstrukata predloženih u cilju boljeg uvida u povezanost shizofrenije i imunoloških alteracija, u drugom delu je razmotren uticaj citokina na pojedine neurotransmiterske sisteme i finalno izneta su zapažanja dobijena iz istraživanja u realnoj kliničkoj situaciji kao i pravci budućih istraživanja.

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Section: Alteracije Citokina Zapažene Kod Obolelih Od Shizofrenije-klunclassified

Schizophrenia and cytokines

Dunjić-Kostić¹,

Pantović-Stefanović²,

Ivković³

et al. 2015

Engrami

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“…In particular, elevated plasma levels of IL-6 have been consistently reported in patients and first-degree relatives with mood disorders (Ganguli et al, 1994;Naudin et al, 1996;Nunes et al, 2005), and correlate with exacerbation of psychotic episodes (Ganguli et al, 1994;Naudin et al, 1996;Lin et al, 1998;Zhang et al, 2002;Kudoh et al, 2003;Nunes et al, 2005). Furthermore, treatment with atypical antipsychotics can alter circulating cytokines (Pollmacher et al, 2000).…”

Section: Mechanism Of Activation Of Nox2 In Neuronsmentioning

confidence: 99%

Does schizophrenia arise from oxidative dysregulation of parvalbumin-interneurons in the developing cortex?

2009

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An imbalance in the redox-state of the brain may be part of the underlying pathophysiology in schizophrenia. Inflammatory mediators, such as IL-6, which can tip the redox balance into a prooxidant state, have been consistently found to be altered in schizophrenia patients. However, the relationship of altered redox-state to altered brain functions observed in the disease has been unclear. Recent data from a pharmacological model of schizophrenia suggest that redox and inflammatory imbalances may be directly linked to the pathophysiology of the disease by alterations in fast-spiking interneurons. Repetitive adult-exposure to the NMDA-R antagonist ketamine increases the levels of the proinflammatory cytokine interleukin-6 in brain which, through activation of the superoxide-producing enzyme NADPH-oxidase (Nox2), leads to the loss of the GABAergic phenotype of PV-interneurons and to decreased inhibitory activity in prefrontal cortex. This effect is not observed after a single exposure to ketamine, suggesting that the first exposure to the NMDA-R antagonist primes the brain such that deleterious effects on PVinterneurons appear upon repetitive exposures. The effects of activation of the IL-6/Nox2 pathway on the PV-interneuronal system are reversible in the adult brain, but permanent in the developing cortex. The slow development of PV-interneurons, while essential for shaping of neuronal circuits during postnatal brain development, increases their vulnerability to deleterious insults that can permanently affect their maturational process. Thus, in individuals with genetic predisposition, the persistent activation of the IL-6/Nox2 pathway may be an environmental factor that tips the redoxbalance leading to schizophrenia symptoms in late adolescence and early adulthood.

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“…[7][8][9] Several genetic variants in cytokines have been associated with the pathogenesis of schizophrenia. [10][11][12][13][14] These findings suggest that cytokines and/or their receptors may be relevant to the development of schizophrenia, though some contradictory results were also reported. 15 IL3 is a major component of immune system and plays a critical role in the development and differentiation of all hematopoietic cell types.…”

Section: Introductionmentioning

confidence: 99%

Association study of CSF2RB with schizophrenia in Irish family and case – control samples

et al. 2007

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Colony stimulating factor 2 receptor, beta (CSF2RB) is the shared subunit of receptors for interleukin 3 (IL3), colony stimulating factor 2 (CSF2) and IL5, and is responsible for the initiation of signal transduction triggered by ligand binding. In our previous study, we showed the evidence that the IL3 gene is associated with schizophrenia and the associations observed are sex-specific and dependent on family history (FH). In this article, we studied 10 singlenucleotide polymorphisms in the CSF2RB gene in the Irish Study of High-Density Schizophrenia Families (ISHDSF) and the Irish Case -Control Study of Schizophrenia (ICCSS), and tested allele and haplotype associations with schizophrenia. Using the pedigree disequilibrium test, we found that two markers (rs11705394 and rs7285064) reached nominal significance. In sex-stratified analyses, for both the markers the association signals were mainly derived from male subjects. In the ICCSS sample, we found that several markers (rs2072707, rs2284031 and rs909486) showed sex-specific and FH-dependent associations with schizophrenia. In multimarker haplotype analyses, both ISHDSF and ICCSS samples showed globally significant associations in multiple linkage disequilibrium (LD) blocks sharing minimal LD. Since CSF2RB is essential for IL3 signaling, the findings that both IL3 and CSF2RB showed sex-specific and FH-dependent associations suggest that the IL3 pathway is involved in schizophrenia.

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Elevated interleukin-2, interleukin-6 and interleukin-8 serum levels in neuroleptic-free schizophrenia: association with psychopathology

Cited by 183 publications

References 59 publications

Schizophrenia and cytokines

Schizophrenia and cytokines

Does schizophrenia arise from oxidative dysregulation of parvalbumin-interneurons in the developing cortex?

Association study of CSF2RB with schizophrenia in Irish family and case – control samples

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