A history of juvenile mild malaria exacerbates chronic stress-evoked anxiety-like behavior, neuroinflammation, and decline of adult hippocampal neurogenesis in mice

Guha, Suman K.; Sarkar, Ishita; Patgaonkar, Mandar; Banerjee, Souvik; Mukhopadhyay, Susanta; Sharma, Shobhona; Pathak, Sulabha; Vaidya, Vidita A.

doi:10.1016/j.jneuroim.2020.577363

Cited by 6 publications

(7 citation statements)

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“…As mentioned before, ageing could affect mice’s behavioral performance ( 33 ) and the stress stimuli induced by the behavioral protocol used in cohort 2 (a larger OFT arena – 50 × 50 × 50 cm) could exemplify this confounding effect observed between the light and dark compartment transitions. Additionally, behavioral alterations have also been described recently in mice with history of juvenile malaria, in response to stress stimulus at adulthood ( 31 ). However, our group was the first to show behavior sequelae in nSEM ( 6 , 18 ) as well as their presence in the short-term (12 days) post-treatment, and their persistence for up to 145 days, in this work.…”

Section: Discussionmentioning

confidence: 90%

“…The classical experimental models of nSM (as, for example, in Swiss Webster mice infected with non-lethal P. yoelii, C57BL/6 with P. chabaudi chabaudi or P. chabaudi adami) have not reproduced the cognitive deficits recorded in man (3,30). However, behavioral changes have been reported as sequelae of nSM in experimental models only recently (6,18,31). De Sousa et al studied the classical experimental model of CM (C57BL/6 infected with P. berghei ANKA) treated with CQ before any clinical signs of CM and observed late behavioral changes and cognitive deficits (6,18).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Dynamics and immunomodulation of cognitive deficits and behavioral changes in non-severe experimental malaria

et al. 2022

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Data recently reported by our group indicate that stimulation with a pool of immunogens capable of eliciting type 2 immune responses can restore the cognitive and behavioral dysfunctions recorded after a single episode of non-severe rodent malaria caused by Plasmodium berghei ANKA. Here we explored the hypothesis that isolated immunization with one of the type 2 immune response-inducing immunogens, the human diphtheria-tetanus (dT) vaccine, may revert damages associated with malaria. To investigate this possibility, we studied the dynamics of cognitive deficits and anxiety-like phenotype following non-severe experimental malaria and evaluated the effects of immunization with both dT and of a pool of type 2 immune stimuli in reversing these impairments. Locomotor activity and long-term memory deficits were assessed through the open field test (OFT) and novel object recognition task (NORT), while the anxiety-like phenotype was assessed by OFT and light/dark task (LDT). Our results indicate that poor performance in cognitive-behavioral tests can be detected as early as the 12th day after the end of antimalarial treatment with chloroquine and may persist for up to 155 days post infection. The single immunization strategy with the human dT vaccine showed promise in reversal of long-term memory deficits in NORT, and anxiety-like behavior in OFT and LDT.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Dynamics and immunomodulation of cognitive deficits and behavioral changes in non-severe experimental malaria

et al. 2022

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“…These alterations may be, however, at least partially due to the inflammatory state of animal during the course of the ongoing infection. In this model, infection also predisposes to enhanced post-stress anxiety-like responses when non-severe malaria occurs at a young age ( Guha et al., 2020 ).…”

Section: Cognitive and Behavioral Sequelae Of Non-severe Malariamentioning

confidence: 99%

Malaria Related Neurocognitive Deficits and Behavioral Alterations

Rosa-Gonçalves

Ribeiro-Gomes

Daniel-Ribeiro

2022

Front. Cell. Infect. Microbiol.

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Typical of tropical and subtropical regions, malaria is caused by protozoa of the genus Plasmodium and is, still today, despite all efforts and advances in controlling the disease, a major issue of public health. Its clinical course can present either as the classic episodes of fever, sweating, chills and headache or as nonspecific symptoms of acute febrile syndromes and may evolve to severe forms. Survivors of cerebral malaria, the most severe and lethal complication of the disease, might develop neurological, cognitive and behavioral sequelae. This overview discusses the neurocognitive deficits and behavioral alterations resulting from human naturally acquired infections and murine experimental models of malaria. We highlighted recent reports of cognitive and behavioral sequelae of non-severe malaria, the most prevalent clinical form of the disease worldwide. These sequelae have gained more attention in recent years and therapies for them are required and demand advances in the understanding of neuropathogenesis. Recent studies using experimental murine models point to immunomodulation as a potential approach to prevent or revert neurocognitive sequelae of malaria.

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“…Researchers have observed high levels of pro-inflammatory cytokines including interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) in the blood of patients suffering from depression and anxiety ( Tang et al, 2018 ; Petralia et al, 2020 ; Primo de Carvalho Alves and Sica da Rocha, 2020 ). In rodent models of depression and anxiety, high levels of pro-inflammatory cytokines and low levels of anti-inflammatory mediators such as IL-10 and IL-4 in the brain are also correlated with the progression of abnormal behaviors ( Wang et al, 2018 ; Walker et al, 2019 ; Zhang et al, 2019 ; Guha et al, 2020 ; Wu et al, 2021 ). Skewing the neuroinflammatory responses in the brain towards an anti-inflammatory state can prevent the progression of abnormal behaviors in animals stimulated with detrimental stress ( Zhao et al, 2016 ; Duan et al, 2020 ; Jing Li et al, 2020 ; Wu et al, 2020 ; Kumar et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Indole-3-Carbinol Selectively Prevents Chronic Stress-Induced Depression-but not Anxiety-Like Behaviors via Suppressing Pro-Inflammatory Cytokine Production and Oxido-Nitrosative Stress in the Brain

Pan

Yang

et al. 2022

Front. Pharmacol.

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Indole-3-carbinol (I3C), a phytochemical enriched in most cruciferous vegetables, has been shown to display various biological activities such as anti-oxidative stress, anti-inflammation, and anti-carcinogenesis. In this study, we investigated the regulatory effect of I3C on chronic stress-induced behavioral abnormalities in mice. Results showed that repeated I3C treatment at the dose of 10, 30, and 60 mg/kg prevented chronic social defeat stress (CSDS)-induced behavioral abnormalities in the tail suspension test, forced swimming test, sucrose preference test, and social interaction test in mice, and did not affect CSDS-induced behavioral abnormalities in the elevated plus maze, light-dark test, and open-field test, suggesting that the I3C treatment selectively prevents the onset of depression- but not anxiety-like behaviors in chronically stressed mice. Further analysis demonstrated that repeated I3C treatment (60 mg/kg, 10 days) prevented CSDS-induced increases in levels of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) mRNA and protein, but did not affect CSDS-induced decreases in levels of IL-4, IL-10, and Ym-1 mRNA and/or protein in the hippocampus and prefrontal cortex, suggesting that I3C can selectively prevent chronic stress-induced pro-inflammatory but not anti-inflammatory responses in the brain. Further analysis showed that repeated I3C treatment (60 mg/kg, 10 days) prevented CSDS-induced increases in levels of nitrite and malondialdehyde (MDA), decreases in contents of glutathione (GSH), and decreases in levels of brain derived neurotrophic factor (BDNF) protein in the hippocampus and prefrontal cortex. These results demonstrated that I3C selectively prevents chronic stress-induced depression-like behaviors in mice likely through suppressing neuroinflammation and oxido-nitrosative stress in the brain.

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A history of juvenile mild malaria exacerbates chronic stress-evoked anxiety-like behavior, neuroinflammation, and decline of adult hippocampal neurogenesis in mice

Cited by 6 publications

References 92 publications

Dynamics and immunomodulation of cognitive deficits and behavioral changes in non-severe experimental malaria

Dynamics and immunomodulation of cognitive deficits and behavioral changes in non-severe experimental malaria

Malaria Related Neurocognitive Deficits and Behavioral Alterations

Indole-3-Carbinol Selectively Prevents Chronic Stress-Induced Depression-but not Anxiety-Like Behaviors via Suppressing Pro-Inflammatory Cytokine Production and Oxido-Nitrosative Stress in the Brain

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