Alterations in gut microbiota contribute to cognitive deficits induced by chronic infection of Toxoplasma gondii

Yang, Xiaoying; Zhou, Yuying; Tan, Shimin; Tian, Xiaokang; Meng, Xianran; Li, Yiling; Zhou, Beibei; Zhao, Guihua; Ge, Xing; He, Cheng; Cheng, Wanpeng; Zhang, Yumei; Zheng, Kuiyang; Yin, Kun; Yu, Yinghua; Pan, Wei

doi:10.1016/j.bbi.2024.04.008

Cited by 3 publications

(1 citation statement)

References 72 publications

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“…Moreover, the effects of a restricted amino acid diet or changes in nutrient levels are not fully understood in the context of Toxoplasma infection. Some data suggest that gut microbiome composition is not drastically altered during chronic Toxoplasma infection ( 45 ), while other studies indicate that alterations in gut microbiota contribute to cognitive deficits induced by chronic Toxoplasma infection ( 46 ). Therefore, the relationship between nutrient availability, diet, gut microbiota, cognitive or neurological alterations, parasite numbers, and pathogenicity remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Selective host autophagy is induced during the intracellular parasite Toxoplasma gondii infection controlling amino acid levels

White,

Angara,

Dias

et al. 2024

mSphere

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Toxoplasma gondii, a widespread parasite, has the ability to infect nearly any nucleated cell in warm-blooded vertebrates. It is estimated that around 2 billion people globally have been infected by this pathogen. Although most healthy individuals can effectively control parasite replication, certain parasites may evade the immune response, establishing cysts in the brain that are refractory to the immune system and resistant to available drugs. For its chronic persistence in the brain, the parasite relies on host cells’ nutrients, particularly amino acids and lipids. Therefore, understanding how latent parasites persist in the brain is crucial for identifying potential drug targets against chronic forms. While shielded within parasitophorous vacuoles (PVs) or cysts, Toxoplasma exploits the host endoplasmic reticulum (ER) metabolism to sustain its persistence in the brain, resulting in host neurological alterations. In this study, we demonstrate that T. gondii disrupts the host ER homeostasis, resulting in the accumulation of unfolded protein within the host ER. The host counters this stress by initiating an autophagic pathway known as ER-phagy, which breaks down unfolded proteins into amino acids, promoting their recycling. Our findings unveil the underlying mechanisms employed by T. gondii to exploit host ER and lysosomal pathways, enhancing nutrient levels during infection. These insights provide new strategies for the treatment of toxoplasmosis. IMPORTANCE Intracellular parasites employ several mechanisms to manipulate the cellular environment, enabling them to persist in the host. Toxoplasma gondii , a single-celled parasite, possesses the ability to infect virtually any nucleated cell of warm-blooded vertebrates, including nearly 2 billion people worldwide. Unfortunately, existing treatments and immune responses are not entirely effective in eliminating the chronic persisting forms of the parasite. This study reveals that T. gondii induces the host’s autophagic pathway to boost amino acid levels in infected cells. The depletion of amino acids, in turn, influences the persistence of the parasite’s chronic forms. Significantly, our investigation establishes the crucial role of host endoplasmic reticulum (ER)-phagy in the parasite’s persistence within the host during latent infection.

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Section: Discussionmentioning

confidence: 99%

Selective host autophagy is induced during the intracellular parasite Toxoplasma gondii infection controlling amino acid levels

White,

Angara,

Dias

et al. 2024

mSphere

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Short chain fatty acids mediates complement C1q pathway alleviation of perioperative neurocognitive disorders

Liu,

Tan,

et al. 2025

Neuropharmacology

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Beyond Auto-Brewery: Why Dysbiosis and the Legalome Matter to Forensic and Legal Psychology

Logan,

Prescott,

LaFata

et al. 2024

Laws

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International studies have linked the consumption of ultra-processed foods with a variety of non-communicable diseases. Included in this growing body of research is evidence linking ultra-processed foods to mental disorders, aggression, and antisocial behavior. Although the idea that dietary patterns and various nutrients or additives can influence brain and behavior has a long history in criminology, in the absence of plausible mechanisms and convincing intervention trials, the topic was mostly excluded from mainstream discourse. The emergence of research across nutritional neuroscience and nutritional psychology/psychiatry, combined with mechanistic bench science, and human intervention trials, has provided support to epidemiological findings, and legitimacy to the concept of nutritional criminology. Among the emergent research, microbiome sciences have illuminated mechanistic pathways linking various socioeconomic and environmental factors, including the consumption of ultra-processed foods, with aggression and antisocial behavior. Here in this review, we examine this burgeoning research, including that related to ultra-processed food addiction, and explore its relevance across the criminal justice spectrum—from prevention to intervention—and in courtroom considerations of diminished capacity. We use auto-brewery syndrome as an example of intersecting diet and gut microbiome science that has been used to refute mens rea in criminal charges. The legalome—microbiome and omics science applied in forensic and legal psychology—appears set to emerge as an important consideration in matters of criminology, law, and justice.

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Alterations in gut microbiota contribute to cognitive deficits induced by chronic infection of Toxoplasma gondii

Cited by 3 publications

References 72 publications

Selective host autophagy is induced during the intracellular parasite Toxoplasma gondii infection controlling amino acid levels

Selective host autophagy is induced during the intracellular parasite Toxoplasma gondii infection controlling amino acid levels

Short chain fatty acids mediates complement C1q pathway alleviation of perioperative neurocognitive disorders

Beyond Auto-Brewery: Why Dysbiosis and the Legalome Matter to Forensic and Legal Psychology

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