Variability in PolyIC induced immune response: Implications for preclinical maternal immune activation models

Careaga, Milo; Taylor, Sandra L.; Chang, C. J.; Chiang, Alex; Ku, Katherine; Berman, Robert F.; Water, Judy Van de; Bauman, Melissa D.

doi:10.1016/j.jneuroim.2018.06.014

Cited by 51 publications

(50 citation statements)

References 76 publications

(95 reference statements)

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“…PolyIC consists of a chain of double stranded inosine (I) and cytidine (C) which can vary in length/molecular weight and demonstrate different immune activating properties in ex vivo paradigms (124, 125 ). Recent in vivo evaluation of PolyIC in a rat model confirms that the same dosage of high-molecular-weight PolyIC can elicit a cytokine response nearly a magnitude in degree higher when compared with low-molecular-weight PolyIC (126). Given that the molecular weight of PolyIC is not reported by most vendors, and that the composition and preparation instructions can differ substantially from vendor to vendor, as well as between batches from the same vendors, different lots of PolyIC likely have dramatically different immunological properties (127).…”

Section: Assessing Validity Of the Mia Modelmentioning

confidence: 97%

Maternal Immune Activation and Autism Spectrum Disorder: From Rodents to Nonhuman and Human Primates

Careaga

Murai

Bauman

2017

Biological Psychiatry

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284

199

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A subset of women who are exposed to infection during pregnancy have an increased risk of giving birth to a child who will later be diagnosed with a neurodevelopmental or neuropsychiatric disorder. Although epidemiology studies have primarily focused on the association between maternal infection and an increased risk of offspring schizophrenia (SZ), mounting evidence indicates that maternal infection may also increase the risk of autism spectrum disorder (ASD). A number of factors, including genetic susceptibility, the intensity and timing of the infection, and exposure to additional aversive postnatal events, may influence the extent to which maternal infection alters fetal brain development and which disease phenotype (ASD; SZ; other neurodevelopmental disorders) is expressed. Preclinical animal models provide a test bed to systematically evaluate the effects of maternal infection on fetal brain development, determine the relevance to human CNS disorders, and to evaluate novel preventative and therapeutic strategies. Maternal immune activation (MIA) models in mice, rats, and nonhuman primates suggest that the maternal immune response is the critical link between exposure to infection during pregnancy and subsequent changes in brain and behavioral development of offspring. However, differences in the type, severity, and timing of prenatal immune challenge paired with inconsistencies in behavioral phenotyping approaches have hindered the translation of preclinical results to human studies. Here we highlight the promises and limitations of the MIA model as a preclinical tool to study prenatal risk factors for ASD, and suggest specific changes to improve reproducibility and maximize translational potential.

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Section: Assessing Validity Of the Mia Modelmentioning

confidence: 97%

Maternal Immune Activation and Autism Spectrum Disorder: From Rodents to Nonhuman and Human Primates

Careaga

Murai

Bauman

2017

Biological Psychiatry

Self Cite

284

199

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“…These concerns stem, in part, from in vitro data demonstrating that Poly IC length varies among manufactures and that this variability may affect the magnitude of immune responses [59,60]. These results have recently been extended to in vivo studies [61] that further emphasize the importance of establishing rigorous reporting guidelines for the MIA model. Perinatal Poly IC exposure typically induces a robust febrile response, a profound increase in cytokine and chemokine production (e.g., IL-1β, IL-6, TNFα, IL-10, CXCL1) [62][63][64], and HPA axis activation [65][66][67].…”

Section: Immune Activationmentioning

confidence: 99%

Maternal immune activation: reporting guidelines to improve the rigor, reproducibility, and transparency of the model

Kentner

Bilbo

Brown

et al. 2018

Neuropsychopharmacol

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210

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The 2017 American College of Neuropychopharmacology (ACNP) conference hosted a Study Group on 4 December 2017, Establishing best practice guidelines to improve the rigor, reproducibility, and transparency of the maternal immune activation (MIA) animal model of neurodevelopmental abnormalities. The goals of this session were to (a) evaluate the current literature and establish a consensus on best practices to be implemented in MIA studies, (b) identify remaining research gaps warranting additional data collection and lend to the development of evidence-based best practice design, and (c) inform the MIA research community of these findings. During this session, there was a detailed discussion on the importance of validating immunogen doses and standardizing the general design (e.g., species, immunogenic compound used, housing) of our MIA models both within and across laboratories. The consensus of the study group was that data does not currently exist to support specific evidence-based model selection or methodological recommendations due to lack of consistency in reporting, and that this issue extends to other inflammatory models of neurodevelopmental abnormalities. This launched a call to establish a reporting checklist focusing on validation, implementation, and transparency modeled on the ARRIVE Guidelines and CONSORT (scientific reporting guidelines for animal and clinical research, respectively). Here we provide a summary of the discussions in addition to a suggested checklist of reporting guidelines needed to improve the rigor and reproducibility of this valuable translational model, which can be adapted and applied to other animal models as well.

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“…Although there is variability in data obtained using mouse models of MIA, notably due to differences in immunogen manufacture (molecular weight, endotoxin contamination, etc. ), timing of immunogen administration, dosage, route of administration, housing conditions, timing of cage cages and mouse strain used (Careaga et al, 2018;Kentner et al, 2019;Kowash et al, 2019), understanding what causes these differences could aid in understanding the mechanisms underlying vulnerability versus resiliency to MIA (Meyer, 2019). In humans, only a subset of pregnant mothers who are exposed to a viral or bacterial infection have offspring who later develop SCZ (Estes et al, 2019).…”

Section: Mia Enhances Risk For Scz By Altering Microglial Functionmentioning

confidence: 99%

The Inflamed Brain in Schizophrenia: The Convergence of Genetic and Environmental Risk Factors That Lead to Uncontrolled Neuroinflammation

Comer

Carrier

Tremblay

et al. 2020

Front. Cell. Neurosci.

152

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Variability in PolyIC induced immune response: Implications for preclinical maternal immune activation models

Cited by 51 publications

References 76 publications

Maternal Immune Activation and Autism Spectrum Disorder: From Rodents to Nonhuman and Human Primates

Maternal Immune Activation and Autism Spectrum Disorder: From Rodents to Nonhuman and Human Primates

Maternal immune activation: reporting guidelines to improve the rigor, reproducibility, and transparency of the model

The Inflamed Brain in Schizophrenia: The Convergence of Genetic and Environmental Risk Factors That Lead to Uncontrolled Neuroinflammation

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