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The Inflammatory Conspiracy in Multiple Sclerosis: A Crossroads of Clues and Insights through Mast Cells, Platelets, Inflammation, Gut Microbiota, Mood Disorders and Stem Cells.
Multiple Sclerosis is a chronic neurological disease characterized by demyelination and axonal loss. This pathology, still largely of unknown etiology, carries within it a complex series of etiopathogenetic components of which it is difficult to trace the origin. An inflammatory state is likely to be the basis of the pathology. Crucial elements of the inflammatory process are the interactions between platelets and mast cells as well as the bacterial component of the intestinal microbiota. In addition, the involvement of mast cells in autoimmune demyelinating diseases has been shown. The present work tries to hang up on that Ariadne's thread which, in the molecular complexity of the interactions between mast cells, platelets, microbiota and inflammation, characterizes Multiple Sclerosis and attempts to bring the pathology back to the causal determinism of psychopathological phenomenology. Therefore, we consider the possibility that the original error of Multiple Sclerosis can be investigated in the genetic origin of the depressive pathology.
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The gut microbiota-brain axis, psychobiotics and its influence on brain and behaviour: A systematic review.
The gut microbiota is the set of microorganisms present in the gut, and it is connected to the central nervous system via the gut-brain axis. Despite there is not a definitive description of the eubiotic microbiota architecture, numerous studies have demonstrated its involvement in human behaviour and its relationship with several pathologies. This is a systematic review about the association between dysbiosis on the gut microbiota and the presence of neurological or neuropsychiatric diseases such as cognitive impairment, Alzheimer's disease, Parkinson's disease, ADHD, and depression. Furthermore, this study analyzes the potential benefits of psychobiotics supplementation for these pathologies. Searches were conducted in the electronic databases PubMed and PsycINFO. 17 articles were included in this review, the majority were published after 2019. The results showed that gut dysbiosis predicts the development of these pathologies and influences their pathogenesis. In addition, it was found that different psychobiotics, mainly dietary fibers and probiotics of the Lactobacillus family, improved different cognitive functions such as cognitive performance and induce a reduced cortisol response. Improvement in different cognitive functions is possible when understanding gut microbiota-brain axis, enteric nervous system, neural-immune system, neuroendocrine system, and central nervous system's relationship.
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The human gut mycobiome and the specific role of Candida albicans: where do we stand, as clinicians?
BACKGROUND: The so-called 'mycobiome' has progressively acquired interest and increased the complexity of our understanding of the human gut microbiota. Several questions are arising concerning the role of fungi (and in particular of Candida albicans), the so-called 'mycobiome', that has been neglected for a long time and only recently gained interest within the scientific community. There is no consensus on mycobiome normobiosis because of its instability and variability. This review aims to raise awareness about this interesting topic and provide a framework to guide physicians faced with such questions. OBJECTIVES: To summarize current knowledge and discuss current and potential implications of the mycobiome in clinical practice. SOURCES: We performed a review of the existing literature in Medline Pubmed. CONTENT: This review identifies several studies showing associations between specific mycobiome profiles and health. Fungi represent a significant biomass within the microbiota and several factors, such as diet, sex, age, co-morbidities, medications, immune status and inter-kingdom interactions, can influence its structure and population. The human gut mycobiota is indeed a key factor for several physiological processes (e.g. training of the immune system against infections) and pathological processes (e.g. immunological/inflammatory disorders, inflammatory bowel diseases, metabolic syndromes). Moreover, the mycobiome (and C. albicans in particular) could influence an even broader spectrum of conditions such as psychiatric diseases (depression, schizophrenia, bipolar disorder) or chronic viral infections (human immunodeficiency virus, hepatitis B virus); moreover, it could be implicated in tumorigenesis. IMPLICATIONS: Candida albicans is a well-known opportunistic pathogen and a major component of the mycobiome but its role in the gastrointestinal tract is still poorly understood. From a potential screening biomarker to a key factor for several pathological processes, its presence could influence or even modify our clinical practice.
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Xiaoyaosan slows cancer progression and ameliorates gut dysbiosis in mice with chronic restraint stress and colorectal cancer xenografts.
Depression is a risk factor for colorectal cancer (CRC) progression. Xiaoyaosan (XYS) is a traditional Chinese medicine prescription for treating depression. Our present study aimed to investigate the effect of XYS on chronic restraint stress (CRS) in mice with CRC xenografts and explore its underlying mechanisms. XYS treatment for 21 consecutive days successfully reduced the tumour volume and tumour weight in mice and prolonged the overall survival time. In addition, the intestinal permeability in the XYS group was significantly improved after administration. The 16S rRNA high-throughput sequencing method was used to sequence stool samples to check the structure and changes of gut bacteria. XYS mainly regulated the abundance of Bacteroides, Lactobacillus, Desulfovibrio and Rikenellaceae. Taken together, these results provide direct strong evidence that XYS effectively improves the progression of CRC in CRS-handled mice, and its efficacy is associated with the modulation of gut dysbiosis. The application of XYS can be a novel therapeutic strategy for CRC patients with depression.
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Gut microbiota-mediated metabolic restructuring aggravates emotional deficits after anesthesia/surgery in rats with preoperative stress.
Patients with preoperative stress are prone to postoperative emotional deficits. However, the underlying mechanisms are largely unknown. Here, we characterize the changes of microbial composition and specific metabolites after anesthesia/surgery in rats with preoperative stress based on 16S rRNA gene sequencing and non-targeted metabolomics technique. Consequently, we found that anesthesia/surgery aggravated anxiety-like and depression-like behaviors in rats under preoperative stress. Microglia were activated and pro-inflammatory cytokines, including interleukin 6 (IL-6) and tumor necrosis factor ɑ (TNF-α) were upregulated after anesthesia/surgery. The postoperative gut microbiota and metabolite composition of rats exposed to preoperative stress differed from those of control rats. Lastly, emotional impairments, metabolic alterations, and neuroinflammation returned normal in antibiotics-treated rats. Our findings provide further evidence that abnormalities in the gut microbiota contribute to postoperative metabolic restructuring, neuroinflammation, and psychiatric deficits in rats under preoperative stress.
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Multi-omics reveal microbial determinants impacting the treatment outcome of antidepressants in major depressive disorder.
BACKGROUND: There is a growing body of evidence suggesting that disturbance of the gut-brain axis may be one of the potential causes of major depressive disorder (MDD). However, the effects of antidepressants on the gut microbiota, and the role of gut microbiota in influencing antidepressant efficacy are still not fully understood. RESULTS: To address this knowledge gap, a multi-omics study was undertaken involving 110 MDD patients treated with escitalopram (ESC) for a period of 12 weeks. This study was conducted within a cohort and compared to a reference group of 166 healthy individuals. It was found that ESC ameliorated abnormal blood metabolism by upregulating MDD-depleted amino acids and downregulating MDD-enriched fatty acids. On the other hand, the use of ESC showed a relatively weak inhibitory effect on the gut microbiota, leading to a reduction in microbial richness and functions. Machine learning-based multi-omics integrative analysis revealed that gut microbiota contributed to the changes in plasma metabolites and was associated with several amino acids such as tryptophan and its gut microbiota-derived metabolite, indole-3-propionic acid (I3PA). Notably, a significant correlation was observed between the baseline microbial richness and clinical remission at week 12. Compared to non-remitters, individuals who achieved remission had a higher baseline microbial richness, a lower dysbiosis score, and a more complex and well-organized community structure and bacterial networks within their microbiota. These findings indicate a more resilient microbiota community in remitters. Furthermore, we also demonstrated that it was not the composition of the gut microbiota itself, but rather the presence of sporulation genes at baseline that could predict the likelihood of clinical remission following ESC treatment. The predictive model based on these genes revealed an area under the curve (AUC) performance metric of 0.71. CONCLUSION: This study provides valuable insights into the role of the gut microbiota in the mechanism of ESC treatment efficacy for patients with MDD. The findings represent a significant advancement in understanding the intricate relationship among antidepressants, gut microbiota, and the blood metabolome. Additionally, this study offers a microbiota-centered perspective that can potentially improve antidepressant efficacy in clinical practice. By shedding light on the interplay between these factors, this research contributes to our broader understanding of the complex mechanisms underlying the treatment of MDD and opens new avenues for optimizing therapeutic approaches. Video Abstract.
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Role of microbiota-derived short-chain fatty acids in nervous system disorders.
During the past decade, accumulating evidence from the research highlights the suggested effects of bacterial communities of the human gut microbiota and their metabolites on health and disease. In this regard, microbiota-derived metabolites and their receptors, beyond the immune system, maintain metabolism homeostasis, which is essential to maintain the host's health by balancing the utilization and intake of nutrients. It has been shown that gut bacterial dysbiosis can cause pathology and altered bacterial metabolites' formation, resulting in dysregulation of the immune system and metabolism. The short-chain fatty acids (SCFAs), such as butyrate, acetate, and succinate, are produced due to the fermentation process of bacteria in the gut. It has been noted remodeling in the gut microbiota metabolites associated with the pathophysiology of several neurological disorders, such as Alzheimer's disease, multiple sclerosis, Parkinson's disease, amyotrophic lateral sclerosis, stress, anxiety, depression, autism, vascular dementia, schizophrenia, stroke, and neuromyelitis optica spectrum disorders, among others. This review will discuss the current evidence from the most significant studies dealing with some SCFAs from gut microbial metabolism with selected neurological disorders.
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Microbiota in anorexia nervosa: potential for treatment.
Anorexia nervosa (AN) is characterised by the restriction of energy intake in relation to energy needs and a significantly lowered body weight than normally expected, coupled with an intense fear of gaining weight. Treatment of AN is currently based on psychological and refeeding approaches, but their efficacy remains limited since 40% of patients after 10 years of medical care still present symptoms of AN. The intestine hosts a large community of microorganisms, called the "microbiota", which live in symbiosis with the human host. The gut microbiota of a healthy human is dominated by bacteria from two phyla: Firmicutes and, majorly, Bacteroidetes. However, the proportion in their representation differs on an individual basis and depends on many external factors including medical treatment, geographical location and hereditary, immunological and lifestyle factors. Drastic changes in dietary intake may profoundly impact the composition of the gut microbiota, and the resulting dysbiosis may play a part in the onset and/or maintenance of comorbidities associated with AN, such as gastrointestinal disorders, anxiety and depression, as well as appetite dysregulation. Furthermore, studies have reported the presence of atypical intestinal microbial composition in patients with AN compared with healthy normal-weight controls. This review addresses the current knowledge about the role of the gut microbiota in the pathogenesis and treatment of AN. The review also focuses on the bidirectional interaction between the gastrointestinal tract and the central nervous system (microbiota-gut-brain axis), considering the potential use of the gut microbiota manipulation in the prevention and treatment of AN.
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Association between microbiome and the development of adverse posttraumatic neuropsychiatric sequelae after traumatic stress exposure.
Patients exposed to trauma often experience high rates of adverse post-traumatic neuropsychiatric sequelae (APNS). The biological mechanisms promoting APNS are currently unknown, but the microbiota-gut-brain axis offers an avenue to understanding mechanisms as well as possibilities for intervention. Microbiome composition after trauma exposure has been poorly examined regarding neuropsychiatric outcomes. We aimed to determine whether the gut microbiomes of trauma-exposed emergency department patients who develop APNS have dysfunctional gut microbiome profiles and discover potential associated mechanisms. We performed metagenomic analysis on stool samples (n = 51) from a subset of adults enrolled in the Advancing Understanding of RecOvery afteR traumA (AURORA) study. Two-, eight- and twelve-week post-trauma outcomes for post-traumatic stress disorder (PTSD) (PTSD checklist for DSM-5), normalized depression scores (PROMIS Depression Short Form 8b) and somatic symptom counts were collected. Generalized linear models were created for each outcome using microbial abundances and relevant demographics. Mixed-effect random forest machine learning models were used to identify associations between APNS outcomes and microbial features and encoded metabolic pathways from stool metagenomics. Microbial species, including Flavonifractor plautii, Ruminococcus gnavus and, Bifidobacterium species, which are prevalent commensal gut microbes, were found to be important in predicting worse APNS outcomes from microbial abundance data. Notably, through APNS outcome modeling using microbial metabolic pathways, worse APNS outcomes were highly predicted by decreased L-arginine related pathway genes and increased citrulline and ornithine pathways. Common commensal microbial species are enriched in individuals who develop APNS. More notably, we identified a biological mechanism through which the gut microbiome reduces global arginine bioavailability, a metabolic change that has also been demonstrated in the plasma of patients with PTSD.
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The microbiota-gut-brain axis in hippocampus-dependent learning and memory: current state and future challenges.
A fundamental shift in neuroscience suggests bidirectional interaction of gut microbiota with the healthy and dysfunctional brain. This microbiota-gut-brain axis has mainly been investigated in stress-related psychopathology (e.g. depression, anxiety). The hippocampus, a key structure in both the healthy brain and psychopathologies, is implicated by work in rodents that suggests gut microbiota substantially impact hippocampal-dependent learning and memory. However, understanding microbiota-hippocampus mechanisms in health and disease, and translation to humans, is hampered by the absence of a coherent evaluative approach. We review the current knowledge regarding four main gut microbiota-hippocampus routes in rodents: through the vagus nerve; via the hypothalamus-pituitary-adrenal-axis; by metabolism of neuroactive substances; and through modulation of host inflammation. Next, we suggest an approach including testing (biomarkers of) the four routes as a function of the influence of gut microbiota (composition) on hippocampal-dependent (dys)functioning. We argue that such an approach is necessary to proceed from the current state of preclinical research to beneficial application in humans to optimise microbiota-based strategies to treat and enhance hippocampal-dependent memory (dys)functions.