Maternal Immune Activation, Cytokines and Autism

Patterson, Paul H.; Xu, Wensi; Smith, Stephen; Devarman, Benjamin E.

doi:10.1007/978-1-60327-489-0_13

Cited by 13 publications

(14 citation statements)

References 102 publications

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“…Murine models add further support for a role of MIA in altering fetal neurodevelopment (Patterson, 2009; Patterson et al, 2009). Many of these studies utilize either a maternal influenza infection or polyinosinic–polycytidylic acid [poly(I:C)] a synthetic toll-like receptor (TLR)-3 agonist that mimics viral infection.…”

Section: Introductionmentioning

confidence: 88%

Maternal immune activation leads to activated inflammatory macrophages in offspring

Onore

Schwartzer

Careaga

et al. 2014

Brain, Behavior, and Immunity

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Several epidemiological studies have shown an association between infection or inflammation during pregnancy and increased risk of autism in the child. In addition, animal models have illustrated that maternal inflammation during gestation can cause autism-relevant behaviors in the offspring; so called maternal immune activation (MIA) models. More recently, permanent changes in T cell cytokine responses were reported in children with autism and in offspring of MIA mice; however, the cytokine responses of other immune cell populations have not been thoroughly investigated in these MIA models. Similar to changes in T cell function, we hypothesized that following MIA, offspring will have long-term changes in macrophage function. To test this theory, we utilized the poly (I:C) MIA mouse model in C57BL/6J mice and examined macrophage cytokine production in adult offspring. Pregnant dams were given either a single injection of 20 mg/kg polyinosinic–polycytidylic acid, poly (I:C), or saline delivered intraperitoneally on gestational day 12.5. When offspring of poly (I:C) treated dams reached 10 weeks of age, femurs were collected and bone marrow-derived macrophages were generated. Cytokine production was measured in bone marrow-derived macrophages incubated for 24 h in either growth media alone, LPS, IL-4/LPS, or IFN-γ/LPS. Following stimulation with LPS alone, or the combination of IFN-γ/LPS, macrophages from offspring of poly (I:C) treated dams produced higher levels of IL-12(p40) (p < 0.04) suggesting an increased M1 polarization. In addition, even without the presence of a polarizing cytokine or LPS stimulus, macrophages from offspring of poly (I:C) treated dams exhibited a higher production of CCL3 (p = 0.05). Moreover, CCL3 levels were further increased when stimulated with LPS, or polarized with either IL-4/LPS or IFN-γ/LPS (p < 0.05) suggesting a general increase in production of this chemokine. Collectively, these data suggest that MIA can produce lasting changes in macrophage function that are sustained into adulthood.

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Section: Introductionmentioning

confidence: 88%

Maternal immune activation leads to activated inflammatory macrophages in offspring

Onore

Schwartzer

Careaga

et al. 2014

Brain, Behavior, and Immunity

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“…However, their role (along with other factors) in triggering a maternal immune activation (MIA) state is rather important, as it might ultimately lead to autism. This notion is supported by several animal studies in which infections were replicated or mimicked (directly and indirectly) to induce an analogous MIA state during pregnancy which eventually lead to behavioural abnormalities (Patterson et al 2008). In human studies, the ability of different pathogens to precipitate similar clinical outcome in the foetus, and the fact that most of these pathogens are limited to specifi c maternal areas (i.e.…”

Section: Danish Health Registersmentioning

confidence: 96%

“…Instead, our fi ndings show an altered immune response with activation of both pro/anti-infl ammatory arms. While accumulating lines of research have suggested a role of pro-infl ammatory cytokines as key players in MIA and the development of ASD (Patterson et al 2008), a specifi c role of anti-infl ammatory cytokines has not been widely investigated. The elevated levels reported in our study (specifi cally IL-10) may represent a compensatory response (Meyer et al 2006;Molloy et al 2006) or rather a more complicated phenomenon interpreted within the integrated and dynamic view of the immune system (Mocellin et al 2004).…”

Section: Limitationsmentioning

confidence: 99%

Amniotic fluid inflammatory cytokines: Potential markers of immunologic dysfunction in autism spectrum disorders

Abdallah

Larsen

Grove

et al. 2011

The World Journal of Biological Psychiatry

159

126

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“…Coe et al [30] concluded from these studies that some immune responses at birth were extremely sensitive to prior prenatal events, while the bidirectional changes also suggested that there may be critical periods in gestation when the same extrinsic events have radically different effects on the fetus. The same group also investigated placental transfer of maternal antibody in either control neonatal squirrel monkeys (63) or animals born to mothers undergoing either a single or 3 periods of disturbance (21 or 29 animals respectively). Levels of IgG were determined in mothers and neonates at parturition.…”

Section: Studies In Other Species and Non-human Primatesmentioning

confidence: 99%

Pre- and Postnatal Influences of Neurohormonal Triggering and Behaviour on the Immune System of Offspring

Gorczynski

Terzioglu

et al. 2011

Advances in Neuroimmune Biology

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It has been realized for some time that exposure of the developing neonate from conception through birth to (toxic) environmental agents can affect the subsequent health and well-being of the offspring. While organogenesis (the first eight weeks of human gestation) is recognized to be a highly susceptible period for the induction of malformations, the fetal/neonatal developmental phases are now acknowledged to be just as sensitive for many well-documented developmental deficits, amongst which are immune-related disorders. In addition, developing predominantly from studies of maternal stress during pregnancy, a growing body of literature now exists to show that changes in the neurohormonal milieu of both mother/infant during pregnancy and weaning can change immune potential of the offspring. Perhaps even more provocative, there is data to suggest that immune changes in the pregnant mother can in turn modify behavior in offspring. The review below provides a framework for consideration of many of the factors contributing to such processes, and their possible mechanism(s) of action.

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Maternal Immune Activation, Cytokines and Autism

Cited by 13 publications

References 102 publications

Maternal immune activation leads to activated inflammatory macrophages in offspring

Maternal immune activation leads to activated inflammatory macrophages in offspring

Amniotic fluid inflammatory cytokines: Potential markers of immunologic dysfunction in autism spectrum disorders

Pre- and Postnatal Influences of Neurohormonal Triggering and Behaviour on the Immune System of Offspring

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