Faecal microbiota transplantation alleviates symptoms of depression in individuals with irritable bowel syndrome: A case series

Collyer, Rhys; Clancy, Annabel; Borody, Thomas J.

doi:10.1016/j.medmic.2020.100029

Cited by 18 publications

(14 citation statements)

References 23 publications

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“…Intraperitoneal injection of ceftriaxone reversed the behavioural changes caused by MPTP and PD faecal microbiota. These results are consistent with previous reports that ceftriaxone could improve the motor dysfunction of PD [ 20 , 22 ].…”

Section: Discussionsupporting

confidence: 94%

Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota

Zhou

Wei

et al. 2021

Oxidative Medicine and Cellular Longevity

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Parkinson’s disease (PD) is a common degenerative disease of the central nervous system. Although some drugs can alleviate the progress of PD, their long-term use will lead to complications, so it is still necessary to find new drugs to delay or cure PD effectively. In view of the difficulty in developing new drugs, it is imperative to discover new functions of existing compounds that could be used to treat PD. In this study, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used to induce PD symptoms in a mouse model. Subsequently, these mice were treated with the antibiotic ceftriaxone. Ceftriaxone alleviated the behavioural and neuropathological changes induced by MPTP, downregulated the expression of glial fibrillary acidic protein (GFAP) and ionised calcium-binding adapter molecule 1 (Iba1) as markers of astroglia and microglia, respectively, and reduced the expression of neuroinflammation-related Toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), and phosphorylated nuclear factor kappa-B (p-NF-κB)/NF-κB in the brain of PD mice. In addition, ceftriaxone reduced the abundance of pathogenic bacteria of the genus Proteus and increased the abundance of probiotic Akkermansia. Finally, ceftriaxone treatment increased the expression of the tight junction proteins zona occludens-1(ZO-1) and occludin in the colon, decreased the expression of the inflammation-related proteins TLR4, MyD88, and NF-κB in the colon, and decreased the serum concentration of the proinflammatory cytokines interleukin-1β (IL-1β), IL-6, and tumour necrosis factor-α (TNF-α). These results indicate that ceftriaxone had a neuroprotective effect on MPTP-induced PD mice, and its neuroprotective effect could be through regulating inflammation and intestinal microbiota. While we showed that ceftriaxone exerts a neuroprotective effect in an MPTP-induced PD mouse model, our findings are limited to the short-term effects of ceftriaxone. Additional work using transgenic mice is required to determine the long-term effects of ceftriaxone. In addition, the dose and frequency of ceftriaxone use should be evaluated.

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Section: Discussionsupporting

confidence: 94%

Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota

Zhou

Wei

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Another small case series brought to light the beneficial effect of FMT on depressed patients diagnosed with IBS via colonoscopy. It is still questionable whether decreased symptomatology was due to FMT or improvement of IBS [ 98 ].…”

Section: Resultsmentioning

confidence: 99%

An Updated Narrative Mini-Review on the Microbiota Changes in Antenatal and Post-Partum Depression

Doroftei

Ilie

Diaconu³

et al. 2022

Diagnostics

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Background: Antenatal depression (AND) and post-partum depression (PPD) are long-term debilitating psychiatric disorders that significantly influence the composition of the gut flora of mothers and infants that starts from the intrauterine life. Not only does bacterial ratio shift impact the immune system, but it also increases the risk of potentially life-threatening disorders. Material and Methods: Therefore, we conducted a narrative mini-review aiming to gather all evidence published between 2018–2022 regarding microflora changes in all three stages of pregnancy. Results: We initially identified 47 potentially eligible studies, from which only 7 strictly report translocations; 3 were conducted on rodent models and 4 on human patients. The remaining studies were divided based on their topic, precisely focused on how probiotics, breastfeeding, diet, antidepressants, exogenous stressors, and plant-derived compounds modulate in a bidirectional way upon behavior and microbiota. Almost imperatively, dysbacteriosis cause cognitive impairments, reflected by abnormal temperament and personality traits that last up until 2 years old. Thankfully, a distinct technique that involves fecal matter transfer between individuals has been perfected over the years and was successfully translated into clinical practice. It proved to be a reliable approach in diminishing functional non- and gastrointestinal deficiencies, but a clear link between depressive women’s gastrointestinal/vaginal microbiota and clinical outcomes following reproductive procedures is yet to be established. Another gut-dysbiosis-driving factor is antibiotics, known for their potential to trigger inflammation. Fortunately, the studies conducted on mice that lack microbiota offer, without a shadow of a doubt, insight. Conclusions: It can be concluded that the microbiota is a powerful organ, and its optimum functionality is crucial, likely being the missing puzzle piece in the etiopathogenesis of psychiatric disorders.

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“…Based on gnotobiotic mouse models, the donor selection may be the key factor, as behavioral and physiological abnormalites seen in patients can be transferred into germ-free mice through microbiota transplantation, 73 thus highlighting not only the necessity to screen in depth potential donors for physical and mental health, but also the potential for treating psychiatric comorbidities of IBS. 96 In conclusion, accumulating data suggest that, in a significant proportion of patients, the microbiota plays an important role in the genesis and maintenance of IBS. The use of personalized dietary approaches, probiotics and other microbiota directed therapies, including FMT, appears to be of therapeutic value, although more clinical data are needed.…”

Section: Microbiota-directed Therapies Of Ibsmentioning

confidence: 91%

Gut Microbiome and Its Role in the Pathophysiology of Irritable Bowel Syndrome

Palma¹,

Berčík²

2021

Acta gastroenterol. latinoam.

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Irritable bowel syndrome is the most common functional gastrointestinal disorder, affecting up to 9% individuals globally. Although the etiology of this syndrome is likely heterogenous, it presents with its hallmark symptoms of abdominal pain and altered intestinal motility. Moreover, it is considered to be a disorder of the gut-brain interaction, and the microbiome has often been implicated as a central player in its pathophysiology. Patients with irritable bowel syndrome display altered composition and function of the gut microbiota compared to healthy controls. Microbiome directed therapies, such as probiotics, antibiotics and fecal microbiome transplantation, appear to be beneficial for both gut symptoms and psychiatric comorbidities. This review aims to recapitulate the available literature on the microbiome contribution to the pathophysiology and symptoms presentation of irritable bowel syndrome, as well as the current literature on microbiome-targeted treatments for this disease.

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Faecal microbiota transplantation alleviates symptoms of depression in individuals with irritable bowel syndrome: A case series

Cited by 18 publications

References 23 publications

Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota

Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota

An Updated Narrative Mini-Review on the Microbiota Changes in Antenatal and Post-Partum Depression

Gut Microbiome and Its Role in the Pathophysiology of Irritable Bowel Syndrome

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