Bacteroides is increased in an autism cohort and induces autism-relevant behavioral changes in mice in a sex-dependent manner

Carmel, Julie; Ghanayem, Nasreen; Mayouf, Rasha; Saleev, Natalia; Chaterjee, Ipsita; Getselter, Dmitriy; Tikhonov, Evgeny; Turjeman, Sondra; Shaalan, Monia; Khateeb, Saleh; Kuzminsky, Alla; Kvetniy-Ferdman, Netta; Kronos, Tanya; Bretler-Zager, Tali; Koren, Omry; Elliott, Evan

doi:10.1038/s41522-023-00469-2

Cited by 9 publications

(4 citation statements)

References 32 publications

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“…However, more recent studies do not support this link, and in fact indicate that dysbiosis in autistic individuals is characterized by elevated levels of Bacteroides spp. which in animal models can worsen behavior [ 256 ]. The increase in this strain is confirmed by meta-analyses using several cohorts, with concomitant elevated IL-6 levels in ASD patients [ 257 ].…”

Section: Mia and Microbiome Dysregulationmentioning

confidence: 99%

“…producing SCFAs [92][93][94] GABA releasing [129] preventing MIA-Induced ASD-relevant deficits in adult offspring [304] preventing parvalbumin-positive neuron loss, increased proinflammatory cytokines levels in maternal serum and fetal brain, and decreased GABA levels [304] intestinal refilling of tryptophan (Bifidobacterium infantis) [120] inducing changes in γ-aminobutyric acid (L. rhamnosus) [107] taking part in maintaining tight junctions between cells [55] preventing the overgrowth of Candida [56] promoting oxytocin levels (L. reuteri) [277] B. fragilis: regulating intestinal barrier integrity [110] lowering Il-6 in colon [110] [259] reducing gut permeability [53] promoting stem cell regeneration and increase mucus secretion in intestines [254] promoting the development of regulatory T cells and IL-22 secretion [255] ⬆ B. fragilis may reduce integrity due to the secreting fragilinase [253] Bacteroides spp. : improving communicative, repetitive, anxiety-like, and sensorimotor behavior associated with ASD in mice (Bacteroides thetaiotaomicron) [110] ⬆ levels in autistic individuals [257] exacerbate social behaviors in mice [256] B. fragilis may reduce integrity due to the secreting fragilinase [253] Bacteroides spp. : improving communicative, repetitive, anxiety-like, and sensorimotor behavior associated with ASD in mice (Bacteroides thetaiotaomicron) [110] Nutrients 2024, 16, 549 23 of…”

Section: Bifidocateriummentioning

confidence: 99%

“…rhamnosus) [107] taking part in maintaining tight junctions between cells [55] preventing the overgrowth of Candida [56] promoting oxytocin levels (L. reuteri) [277] B. fragilis: regulating intestinal barrier integrity [110] lowering Il-6 in colon [110] [259] reducing gut permeability [53] promoting stem cell regeneration and increase muc secretion in intestines [254] promoting the development of regulatory T cells an IL-22 secretion [255] ⬆ B. fragilis may reduce integrity due to the secretin fragilinase [253] Bacteroides spp. : improving communicative, repetitive, anxiety-like and sensorimotor behavior associated with ASD in mice (Bacteroides thetaiotaomicron) [110] ⬆ levels in autistic individuals [257] exacerbate social behaviors in mice [256] levels in autistic individuals [257] exacerbate social behaviors in mice [256] Dysbiosis can increase inflammation in the mother's and children's bodies, with a high-fat diet, maternal obesity, or antibiotic therapy likely to disrupt the composition of the microflora. However, further well-designed studies are needed due to the limitation and inconclusiveness of the studies so far, resulting from the inability to verify the authenticity of the cases analyzed and conclusively determine whether the source of the disruption is genetic or an external factor.…”

Section: Bifidocateriummentioning

confidence: 99%

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Between Dysbiosis, Maternal Immune Activation and Autism: Is There a Common Pathway?

Suprunowicz,

Tomaszek,

Urbaniak

et al. 2024

Nutrients

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Autism spectrum disorder (ASD) is a neuropsychiatric condition characterized by impaired social interactions and repetitive stereotyped behaviors. Growing evidence highlights an important role of the gut–brain–microbiome axis in the pathogenesis of ASD. Research indicates an abnormal composition of the gut microbiome and the potential involvement of bacterial molecules in neuroinflammation and brain development disruptions. Concurrently, attention is directed towards the role of short-chain fatty acids (SCFAs) and impaired intestinal tightness. This comprehensive review emphasizes the potential impact of maternal gut microbiota changes on the development of autism in children, especially considering maternal immune activation (MIA). The following paper evaluates the impact of the birth route on the colonization of the child with bacteria in the first weeks of life. Furthermore, it explores the role of pro-inflammatory cytokines, such as IL-6 and IL-17a and mother’s obesity as potentially environmental factors of ASD. The purpose of this review is to advance our understanding of ASD pathogenesis, while also searching for the positive implications of the latest therapies, such as probiotics, prebiotics or fecal microbiota transplantation, targeting the gut microbiota and reducing inflammation. This review aims to provide valuable insights that could instruct future studies and treatments for individuals affected by ASD.

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Section: Mia and Microbiome Dysregulationmentioning

confidence: 99%

Section: Bifidocateriummentioning

confidence: 99%

Section: Bifidocateriummentioning

confidence: 99%

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Between Dysbiosis, Maternal Immune Activation and Autism: Is There a Common Pathway?

Suprunowicz,

Tomaszek,

Urbaniak

et al. 2024

Nutrients

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“…At the end of the test, the number of marbles that are 2/3 buried by the subject is used to measure the repetitive digging behavior. Autistic models have a high tendency to bury more balls than wild-type and healthy animals [59,62].…”

Section: Marble Buryingmentioning

confidence: 99%

Animal Models of Autistic-Like Behavior: Is the Time for a Scoring System with More Accurate Definitions?

Ornoy,

Echefu,

Becker

2024

Preprint

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Appropriate animal models of human diseases are a cornerstone in the advancement of science and medicine. To create animal models of neuropsychiatric and neurobehavioral diseases such as ASD necessitates the development of sufficient neurobehavioral measuring tools to translate human behavior to expected measurable behavioral features in animals. Indeed, at least in rodents, adequate neurobehavioral and neurological tests have been developed. Since ASD is characterized by a number of specific behavioral trends with significant severity, animal models of autistic-like behavior have to demonstrate the specific characteristic features, namely impaired social interactions, and communication, restricted, repetitive behavioral patterns with association to several additional impairments such as somatosensory, motor and memory impairments. Thus, an appropriate model must show behavioral impairment of a minimal number of neurobehavioral characteristics using an adequate number of behavioral tests. The proper animal models enable the study of ASD like-behavior from the etiologic, pathogenetic and therapeutic aspects. From the etiologic aspects, models have been developed by the use of immunogenic substances like polyinosinic-polycytidylic acid (PolyIC), Lipopolysaccharide (LPS) and propionic acid or other well-documented immunogens or pathogens, like mycobacterium tuberculosis. Another approach is the use of chemicals like valproic acid, Polychlorinated biphenyls (PCBs), organophosphate pesticides - chlorpyrifos (CPF) and others. These substances were administered either prenatally, generally after the period of major organogenesis, or, especially in rodents, during the early postnatal life. In addition, using modern genetic manipulation methods, genetic models have been created of almost all human genetic diseases that are manifested by autistic like behavior (i.e. fragile X, Rett syndrome, SHANK gene mutation Neuroligin genes and others). Ideally, we should not only evaluate the different behavioral modes affected by the ASD-like behavior but also assess the severity of the behavioral deviations by an appropriate scoring system, as applied to humans.

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Investigating the Effect of Capric Acid on Antibiotic‐Induced Autism‐Like Behavior in Rodents

Shekhar,

Thakur

2024

Developmental Neurobiology

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Owing to the high prevalence of gastrointestinal dysfunction in patients, the gut–brain axis is considered to play a vital role in neurodevelopment diseases. Recent pieces of evidence have pointed to the usage of antibiotics at an early developmental stage to be a causative factor in autism due to its ability to induce critical changes in the gut microbiota. The purpose of the study is to determine the neuroprotective effect of capric acid (CA) on autism in antibiotic‐induced gut dysbiosis in rodents. In this study, the effect of CA was observed in penicillin V (31 mg/kg, p.o.) exposed animals by evaluating their autism‐like behavioral and biochemical parameters. The establishment of gut dysbiosis was confirmed by 16 RNA sequencing, and behavioral tests were performed. Subsequently, oxidative stress, cytokine levels, and mitochondrial complex activities in the hippocampus and prefrontal cortex were analyzed. It was observed that the administration of penicillin V during the perinatal period produced gut dysbiosis and long‐lasting changes in social behavior with symptoms of anxiety and depression and impaired learning and memory. Treatment with penicillin V also produced oxidative stress, mitochondrial dysfunction, and inflammation in the hippocampus and prefrontal cortex. Treatment with CA produced a positive effect on the alterations with maximum effects evident at 400 mg/kg, p.o. through amelioration of behavioral as well as biochemical changes. The current study concluded that CA could act as a likely candidate for the treatment and management of autism via modulation of gut dysbiosis‐induced neurobehavioral parameters, oxidative stress, mitochondrial dysfunction, and inflammatory markers.

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Bacteroides is increased in an autism cohort and induces autism-relevant behavioral changes in mice in a sex-dependent manner

Cited by 9 publications

References 32 publications

Between Dysbiosis, Maternal Immune Activation and Autism: Is There a Common Pathway?

Between Dysbiosis, Maternal Immune Activation and Autism: Is There a Common Pathway?

Animal Models of Autistic-Like Behavior: Is the Time for a Scoring System with More Accurate Definitions?

Investigating the Effect of Capric Acid on Antibiotic‐Induced Autism‐Like Behavior in Rodents

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