Maternal immune activation with staphylococcal enterotoxin A produces unique behavioral changes in C57BL/6 mouse offspring

Glass, Ruthy M; Norton, Stata; Fox, Nicholas W.; Kusnecov, Alexander W.

doi:10.1016/j.bbi.2018.05.005

Cited by 37 publications

(25 citation statements)

References 68 publications

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“…For instance, no correlation was found in peripheral and cerebrospinal fluid pro-inflammatory markers in people with ASD (Pardo et al, 2017), suggesting that peripheral markers might not optimally reflect the immune status of the CNS. In fact, basic research addressing the role of MIA in murine models supports the notion that behavioral and immunological effects during MIA are selectively dependent on the animal's strain (Schwartzer et al, 2013) and selective pro-inflammatory trigger (Glass, Norton, Fox, & Kusnecov, 2019;Oskvig, Elkahloun, Johnson, Phillips, & Herkenham, 2012). We expect that such scenario might be recapitulated in people with ASD (Figures 2 and 3; Table 2).…”

Section: Sys Temi C and Centr Al Pro -Infl Ammatory Profile S Reg Umentioning

confidence: 75%

Potential role of primed microglia during obesity on the mesocorticolimbic circuit in autism spectrum disorder

Trujillo-Villarreal

Cárdenas-Tueme²,

Maldonado-Ruiz

et al. 2020

Journal of Neurochemistry

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Section: Sys Temi C and Centr Al Pro -Infl Ammatory Profile S Reg Umentioning

confidence: 75%

Potential role of primed microglia during obesity on the mesocorticolimbic circuit in autism spectrum disorder

Trujillo-Villarreal

Cárdenas-Tueme²,

Maldonado-Ruiz

et al. 2020

Journal of Neurochemistry

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“…Strong evidence indicates that LPS exposure during late embryogenesis could also result in noncognitive behavioral abnormalities in pre‐ or adult, such as altered anxiety‐like and depressive‐like behaviors and locomotor activity, prepulse inhibition deficits, and impaired species‐typical behaviors (hoarding and nesting; Asiaei, Solati, & Salari, ; Enayati et al, ; Fortier et al, ; Glass et al, ; Golan, Stilman, Lev, & Huleihel, ; Hsueh et al, ; Penteado et al, ; Wischhof et al, ). But it is noteworthy that these studies varied with respect to different methodology used, making it difficult to compare across studies.…”

Section: Discussionmentioning

confidence: 99%

“…Bacterial infections have a high prevalence in women of reproductive age. Increasing evidence indicates that modifications of the “in utero” environment due to maternal bacterial infection can result in cognitive and behavioral disorders in pre‐ or adult offspring, such as impairments in spatial learning and memory (Batinic et al, ; Chlodzinska, Gajerska, Bartkowska, Turlejski, & Djavadian, ; Glass, Norton, Fox, & Kusnecov, ; Simões et al, ) and object recognition (Glass et al, ; Wischhof, Irrsack, Osorio, & Koch, ), increased locomotor activity (Batinic et al, ; Glass et al, ) and anxiety (Enayati et al, ; Glass et al, ; Hsueh et al, ; Penteado et al, ) and decreased prepulse inhibition of acoustic startle (Fortier, Luheshi, & Boksa, ; Glass et al, ; Wischhof et al, ) and social behaviors (Glass et al, ; Hsueh et al, ). Lipopolysaccharide (LPS) injection in the pregnancy is a widely accepted mouse model of maternal bacterial infection.…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer‐like behavioral and neuropathological changes in CD‐1 mice

et al. 2020

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Introduction Infections could contribute to Alzheimer's disease (AD) neuropathology in human. However, experimental evidence for a causal relationship between infections during the prenatal phase and the onset of AD is lacking. Methods CD‐1 mothers were intraperitoneally received lipopolysaccharide (LPS) with two doses (25 and 50 μg/kg) or normal saline every day during gestational days 15–17. A battery of behavioral tasks was used to assess the species‐typical behavior, sensorimotor capacity, anxiety, locomotor activity, recognition memory, and spatial learning and memory in 1‐, 6‐, 12‐, 18‐, and 22‐month‐old offspring mice. An immunohistochemical technology was performed to detect neuropathological indicators consisting of amyloid‐β (Aβ), phosphorylated tau (p‐tau), and glial fibrillary acidic protein (GFAP) in the hippocampus. Results Compared to the same‐aged controls, LPS‐treated offspring had similar behavioral abilities and the levels of Aβ42, p‐tau, and GFAP at 1 and 6 months old. From 12 months onward, LPS‐treated offspring gradually showed decreased species‐typical behavior, sensorimotor ability, locomotor activity, recognition memory, and spatial learning and memory, and increased anxieties and the levels of Aβ42, p‐tau, and GFAP relative to the same‐aged controls. Moreover, this damage effect (especially cognitive decline) persistently progressed onwards. The changes in these neuropathological indicators significantly correlated with impaired spatial learning and memory. Conclusions Prenatal exposure to low doses of LPS caused AD‐related features including behavioral and neuropathological changes from midlife to senectitude.

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“…During brain development, the autocrine and paracrine signaling via cytokines regulates neuronal migration, growth, function and survival. Therefore, the MIA-evoked cytokine imbalance significantly affects developmental processes [3][4][5]. Throughout prenatal exposure to inflammation, there are apparent links between ASD and penetration of pro-inflammatory agents into the developing brain [6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Maternal Immune Activation Induces Neuroinflammation and Cortical Synaptic Deficits in the Adolescent Rat Offspring

Cieślik

Gąssowska-Dobrowolska

Jęśko

et al. 2020

IJMS

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Maternal immune activation (MIA), induced by infection during pregnancy, is an important risk factor for neuro-developmental disorders, such as autism. Abnormal maternal cytokine signaling may affect fetal brain development and contribute to neurobiological and behavioral changes in the offspring. Here, we examined the effect of lipopolysaccharide-induced MIA on neuro-inflammatory changes, as well as synaptic morphology and key synaptic protein level in cerebral cortex of adolescent male rat offspring. Adolescent MIA offspring showed elevated blood cytokine levels, microglial activation, increased pro-inflammatory cytokines expression and increased oxidative stress in the cerebral cortex. Moreover, pathological changes in synaptic ultrastructure of MIA offspring was detected, along with presynaptic protein deficits and down-regulation of postsynaptic scaffolding proteins. Consequently, ability to unveil MIA-induced long-term alterations in synapses structure and protein level may have consequences on postnatal behavioral changes, associated with, and predisposed to, the development of neuropsychiatric disorders.

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Maternal immune activation with staphylococcal enterotoxin A produces unique behavioral changes in C57BL/6 mouse offspring

Cited by 37 publications

References 68 publications

Potential role of primed microglia during obesity on the mesocorticolimbic circuit in autism spectrum disorder

Potential role of primed microglia during obesity on the mesocorticolimbic circuit in autism spectrum disorder

Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer‐like behavioral and neuropathological changes in CD‐1 mice

Maternal Immune Activation Induces Neuroinflammation and Cortical Synaptic Deficits in the Adolescent Rat Offspring

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