What Part Of The Brain Does Myasthenia Gravis Affect – Hesperetin ameliorated the inhibition of neuronal and oligodendroglial differentiation phenotypes caused by deletion of Rab2b, a gene product implicated in autism spectrum disorder.
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What Part Of The Brain Does Myasthenia Gravis Affect
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Effects Of Intravascular Photobiomodulation On Motor Deficits And Brain Perfusion Images In Intractable Myasthenia Gravis: A Case Report
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By Giuseppe Schirò Giuseppe Schirò Scilit Preprints.org Google Scholar 1, †, Salvatore Iacono Salvatore Iacono Scilit Preprints.org Google Scholar 1, *, †and Carmela Rita Balistreri Carmela Bali Ritastreri Scilit Preprints.org Google Scholar 2
Adult Brain Tumors: Video, Anatomy & Definition
Cellular and Molecular Laboratory, Department of Biomedicine, Neuroscience and Advanced Diagnostics (BiND), University of Palermo, 90127 Palermo, Italy
Received: 6 February 2023 / Revised: 5 March 2023 / Accepted: 7 March 2023 / Published: 10 March 2023
Myasthenia gravis (MG) is an autoimmune neuromuscular disease characterized by persistent weakness of skeletal muscles. Although antibodies against components of the neuromuscular junction have been recognized, the pathogenesis of MG remains unclear, despite its widely known multifactorial nature. However, it has recently been suggested that perturbation of the human microbiota contributes to the pathogenesis and clinical course of MG. Therefore, some products derived from commensal flora have been shown to have anti-inflammatory effects, while others have pro-inflammatory properties. Furthermore, MG patients, compared with age-matched controls, show a distinctive composition of the oral and intestinal microbiota, with a typical increase in Streptococcus and Bacteroides and a decrease in Clostridia, as well as a decrease in short chain fatty acids. Furthermore, restoration of gut microbiota dysbiosis after probiotic administration, followed by symptomatic improvement in MG cases, has been demonstrated. To highlight the role of the oral and intestinal microbiota in the pathogenesis and clinical course of MG, current evidence has been summarized and reviewed here.
The human microbiota includes the entire microbial population present in the human body and is mainly represented by the intestinal microbiota. Bacteria are the main components of the intestinal microbiota, but protists, archaea and viruses represent other components, although they are present in smaller numbers [1]. They are mainly represented by Firmicutes, Bacteroidetes and Actinobacteria, which represent more than 90% of intestinal bacteria and are essential for maintaining homeostasis of the entire intestinal microbiota [2]. Although there are countless possible combinations, the existence of a limited number of balanced symbiotic states between host and bacteria has been demonstrated. Thus, the existence of three different types of bacteria was observed, each resulting from changes in the levels of one of the following genera: Bacteroides, Prevotella and Ruminococcus [1]. The integrity of the gut microbiota ensures many host physiological processes, such as intestinal barrier function, digestion, metabolism of dietary factors, and vitamin biosynthesis. Therefore, the human microbiome has many functions; In particular, its immunomodulatory function and bidirectional interaction with the central nervous system (CNS) have received much attention in recent decades. Clostridia represent 95% of the Firmicutes phylum that reside in the gut microbiota and are major producers of short-chain fatty acids (SCFAs) through fermentation of proteins and carbohydrates. Notably, SCFAs (e.g., propionate and butyrate) support the differentiation of naïve CD4+ T cells into CD4+ Foxp3+ regulatory T cells (Tregs) by stimulating histone H3 acetylation at the promoter of the Foxp3 gene regulates anti-inflammatory responses. via G. -associated protein receptor 43 [3]. Furthermore, the interaction between the gut microbiota and the immune system also regulates the production of immunoglobulins, especially mucosal IgA. In fact, if the presence of bacteria is reduced, the local antibody response is also reduced. This probably depends on IgA production, which stimulates the microbiota to invade Peyer’s patches, providing positive reinforcement for IgA production [4]. Furthermore, circulating SCFAs can regulate the permeability of endothelial tight junctions, improving the integrity of the blood-brain barrier (BBB). The relationship between the gut microbiota and the central nervous system is known as the microbiome-brain-gut (MGB) axis, a concept first proposed in 2012 [5]. It has been shown that this close relationship is also mediated by neuroanatomical structures that exist between the brain and intestines, and through enteric nerves located in the intestinal wall [5]. From this perspective, information about the gut can be transmitted to the brain via the vagus nerve, with a response through its descending branch, thereby regulating intestinal activity. Furthermore, another component of the MGB axis is the neuroendocrine axis, represented by the hypothalamic-pituitary-adrenal (HPA) axis. It allows the regulation of the main pathway in communication between the gut and the brain under stressful conditions [6]. HPA determines changes in the composition and function of intestinal microorganisms through its activity. Dysfunctions in the HPA have been shown to play an important role in the pathogenesis of neuropsychiatric diseases. Precisely, HPA mediates the activation of inflammatory signaling pathways by releasing inflammatory mediators, such as tumor necrosis factor α (TNF-α), interferon-γ (IFN- γ) and interleukin 6 (IL-6) [7] . In turn, these mediators may contribute to the destruction of BBB integrity and the development of brain diseases, through systemic circulation and damage to the intestinal mucosal barrier. Furthermore, the inflammation-induced HPA response also influences glucocorticoid secretion [8], which in turn activates intestinal function and the production of pro-inflammatory factors [9]. This vicious cycle also causes activation of intestinal immune cells, such as T helper (Th) 17 cells and natural killer cells that can migrate to the brain and cause neuroinflammation [ ten]. Conversely, neuroinflammation also alters intestinal bacterial composition, which then stimulates intestinal immune cells and microbiota-derived metabolites that play a role in regulating the two-way pathway This is through inflammatory signals.
Myasthenia Gravis: Frequently Asked Questions
Due to the immunomodulatory function of the gut microbiota, alterations of the commensal microbiota (i.e. dysbiosis) have recently attracted increasing interest in the pathogenic role of them in immune-mediated diseases. Indeed, dysbiosis is characterized by disruption of host-microbe interactions and is associated with low-grade inflammation, metabolic syndrome, gastrointestinal infections, and inflammatory bowel disease [ 11 , 12, 13, 14]. Notably, a decreased Firmicutes/Bacteroidetes ratio (F/B ratio) due to an increase in the Bacteroidetes phylum has been found to be associated with inflammatory alterations of the gut microbiota in autoimmune diseases. such as systemic lupus erythematosus and systemic sclerosis. . . , Sjogren’s syndrome, antiphospholipid antibody syndrome, multiple sclerosis (MS) and myasthenia gravis (MG), while changes in the F/B ratio are inconsistent with obesity, some of which authors found a decrease while others found an increase [15, 16, 17, 18]. . Although the gut microbiota has received much attention, the oral microbiota has been overlooked. It is estimated that between 500 and 700 different species inhabit the oral cavity, and among them Streptococcus mitis is the most common [19, 20]. However, the composition of the oral microbiota varies widely depending on the oral habitat (e.g., tongue, cheeks, teeth), as well as the presence of exogenous pathogens and/or growth overrepresentation of the previously existing oral microbiota [19, 21]. Although the role of the oral microbiota in MG is largely unexplored, its involvement in the pathogenesis of autoimmune diseases is intriguing. In fact, an increase in Staphylococcus, Actinomyces and Bacteroides genera and a decrease in Lactobacillus were recently found in the oral cavity of patients with MS [22]. MG is a neuromuscular autoimmune disease characterized by immune-mediated destruction of the neuromuscular junction (NMJ). Although antibodies against components of the neuromuscular junction have been recognized, the pathogenesis of MG remains unclear and may be multifactorial [23]. Based on emerging evidence of the role of the microbiota in the pathogenesis of other autoimmune diseases such as MS, it has recently been suggested that perturbation of the human microbiome contributes to the pathogenesis and Clinical course of MG. Therefore, some products derived from commensal flora have been shown to have anti-inflammatory effects, while others have pro-inflammatory properties.
Here, we sought to elucidate the relationship between the oral and intestinal microbiota and the pathogenesis or disease course of MG, summarizing and reviewing the current evidence. In the chapters that follow, real-world studies explore disturbances in the gut and oral microbiota.
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