scholarly journals Influência da Disbiose na Patologia do Couro Cabeludo

2021 ◽  
Vol 79 (4) ◽  
pp. 309-314
Author(s):  
Francisca Morgado ◽  
Rui Oliveira Soares

In recent years, several studies have demonstrated the involvement of the intestinal microbiota in immune-mediated diseases such as diabetes, ulcerative colitis, and multiple sclerosis. There are few data on the follicular microbiome and its role in the pathogenesis of scalp diseases. Some studies show influence of dysbiosis on these diseases, and manipulation of the microbiome may represent a possible therapeu- tic option. This article reviews current knowledge regarding the impact of dysbiosis on dermatological diseases of the scalp, such as seborrheic dermatitis, psoriasis, alopecia areata, androgenetic alopecia, lichen planus pilaris, frontal fibrosing alopecia and decalvant folliculitis. A broader understanding of this may suggest additional treatments beyond conventional therapies.

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Carlos Magno da Costa Maranduba ◽  
Sandra Bertelli Ribeiro De Castro ◽  
Gustavo Torres de Souza ◽  
Cristiano Rossato ◽  
Francisco Carlos da Guia ◽  
...  

Many immune-based intestinal disorders, such as ulcerative colitis and Crohn’s disease, as well as other illnesses, may have the intestines as an initial cause or aggravator in the development of diseases, even apparently not correlating directly to the intestine. Diabetes, obesity, multiple sclerosis, depression, and anxiety are examples of other illnesses discussed in the literature. In parallel, importance of the gut microbiota in intestinal homeostasis and immunologic conflict between tolerance towards commensal microorganisms and combat of pathogens is well known. Recent researches show that the immune system, when altered by the gut microbiota, influences the state in which these diseases are presented in the patient directly and indirectly. At the present moment, a considerable number of investigations about this subject have been performed and published. However, due to difficulties on correlating information, several speculations and hypotheses are generated. Thus, the present review aims at bringing together how these interactions work—gut microbiota, immune system, and their influence in the neuroimmune system.


2015 ◽  
Vol 6 (2) ◽  
pp. 173-179 ◽  
Author(s):  
Y. Vandenplas

This review summarises how the composition of the gastro-intestinal microbiota depends on pre- and postnatal factors, and birth itself. The impact of method of delivery, feeding during infancy and medications, such as antibiotics and anti-acid medication, on the composition of the gastro-intestinal microbiota has clearly been shown. However, the duration of the impact of these factors is not well established. The gastro-intestinal microbiome composition is associated with many auto-immune mediated diseases. Although causality has not been obviously demonstrated, there is a strong tendency in this direction. Nevertheless, results of the manipulation of the gastro-intestinal microbiome composition in these conditions are often disappointing. A better understanding on factors determining the longterm composition of the gastro-intestinal microbiome and its health consequences are a priority research topic. A better understanding of the association between the microbiome and the immune system may have a tremendous impact on general health.


Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1716
Author(s):  
Christophe Espírito Santo ◽  
Catarina Caseiro ◽  
Maria João Martins ◽  
Rosário Monteiro ◽  
Inês Brandão

The gut microbiota is often mentioned as a “forgotten organ” or “metabolic organ”, given its profound impact on host physiology, metabolism, immune function and nutrition. A healthy diet is undoubtedly a major contributor for promoting a “good” microbial community that turns out to be crucial for a fine-tuned symbiotic relationship with the host. Both microbial-derived components and produced metabolites elicit the activation of downstream cascades capable to modulate both local and systemic immune responses. A balance between host and gut microbiota is crucial to keep a healthy intestinal barrier and an optimal immune homeostasis, thus contributing to prevent disease occurrence. How dietary habits can impact gut microbiota and, ultimately, host immunity in health and disease has been the subject of intense study, especially with regard to metabolic diseases. Only recently, these links have started to be explored in relation to lung diseases. The objective of this review is to address the current knowledge on how diet affects gut microbiota and how it acts on lung function. As the immune system seems to be the key player in the cross-talk between diet, gut microbiota and the lungs, involved immune interactions are discussed. There are key nutrients that, when present in our diet, help in gut homeostasis and lead to a healthier lifestyle, even ameliorating chronic diseases. Thus, with this review we hope to incite the scientific community interest to use diet as a valuable non-pharmacological addition to lung diseases management. First, we talk about the intestinal microbiota and interactions through the intestinal barrier for a better understanding of the following sections, which are the main focus of this article: the way diet impacts the intestinal microbiota and the immune interactions of the gut–lung axis that can explain the impact of diet, a key modifiable factor influencing the gut microbiota in several lung diseases.


Author(s):  
Emanuele Rinninella ◽  
Marco Cintoni ◽  
Pauline Raoul ◽  
Antonio Gasbarrini ◽  
Maria Cristina Mele

The interactions between diet, gut microbiota, and irritable bowel syndrome (IBS) have many complex mechanisms that are not fully understood. Food additives are one component of the modern human diet that deserves attention from science and government policies. This review aims at identifying the current knowledge about the impact of food additives on gut microbiota and their potential role in the development of IBS. To date, few data on the effect of food additives on gut microbiota in IBS patients are available. However, exposure to food additives could induce the dysbiosis and dysregulation of gut homeostasis with an alteration of the gut barrier and activation of the immune response. These microbial changes could exacerbate the gut symptoms associated with IBS, such as visceral pain, low-grade inflammation, and changes in bowel habits. Some additives (polyols) are excluded in the low fermentable oligo-, di- and monosaccharide, and polyol (FODMAP), diets for IBS patients. Even if most studies have been performed in animals, and human studies are required, many artificial sweeteners, emulsifiers, and food colorants could represent a potential hidden driver of IBS, through gut microbiota alterations. Consequently, food additives should be preventively avoided in the diet as well as dietary supplements for patients with IBS.


Diseases ◽  
2020 ◽  
Vol 8 (3) ◽  
pp. 33
Author(s):  
Hannah M. Kohl ◽  
Andrea R. Castillo ◽  
Javier Ochoa-Repáraz

There is an increasing interest in the intestinal microbiota as a critical regulator of the development and function of the immune, nervous, and endocrine systems. Experimental work in animal models has provided the foundation for clinical studies to investigate associations between microbiota composition and function and human disease, including multiple sclerosis (MS). Initial work done using an animal model of brain inflammation, experimental autoimmune encephalomyelitis (EAE), suggests the existence of a microbiota–gut–brain axis connection in the context of MS, and microbiome sequence analyses reveal increases and decreases of microbial taxa in MS intestines. In this review, we discuss the impact of the intestinal microbiota on the immune system and the role of the microbiome–gut–brain axis in the neuroinflammatory disease MS. We also discuss experimental evidence supporting the hypothesis that modulating the intestinal microbiota through genetically modified probiotics may provide immunomodulatory and protective effects as a novel therapeutic approach to treat this devastating disease.


2018 ◽  
Vol 24 (3) ◽  
pp. 178-187 ◽  
Author(s):  
Maria A. Ron

SUMMARYMultiple sclerosis (MS), an immune-mediated demyelinating condition, is the most common neurological disease affecting young adults in the UK. It has a high psychiatric comorbidity and over half of patients have some degree of cognitive impairment that adds to the burden of disability. This article reviews the psychiatric and cognitive manifestations of MS and their detection and treatment. Recent advances in the treatment of the disease are briefly reviewed and the impact of disease-modifying therapies on psychiatric morbidity and cognitive impairment is discussed.LEARNING OBJECTIVES•Understand the psychiatric morbidity in MS and its biological counterparts•Understand the cognitive impairment and its biological counterparts•Become familiar with the detection and treatment of the psychiatric and cognitive manifestations of MSDECLARATION OF INTERESTNone.


2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S010-S011
Author(s):  
E Brand ◽  
Y Laenen ◽  
F van Wijk ◽  
M de Zoete ◽  
B Oldenburg

Abstract Background The pathogenesis of inflammatory bowel disease (IBD) is thought to result from an interplay between microbiota, the immune system and the environment in genetically susceptible hosts. Immunoglobulin A (IgA) produced by the immune system can be specifically directed against bacteria. The IgA-coating pattern of intestinal bacteria thus reflects interactions between the immune system and specific bacteria. Studying IBD in twins, concordant and discordant for IBD, reduces the impact of genetic predisposition and childhood exposures and therefore offers the unique opportunity to focus on other factors such as intestinal microbiota composition and immune-interactions in IBD. Methods Faecal samples from twin pairs discordant for Crohn’s disease (CD) or ulcerative colitis (UC) were collected. Employing fluorescence-activated cell sorting, IgA+ and IgA− bacteria from the intestinal microbiota were sorted. Subsequently, (1) the total, (2) IgA+ and (3) IgA− microbial composition was determined by 16S rRNA sequencing (IgA-SEQ). We estimated the relative IgA coating per bacterial species by dividing the abundance of that species in the IgA+ fraction over the abundance in the IgA- fraction, representing the IgA coating index. Linear discriminant analyses were performed with LefSE. Results We included 31 twin pairs (62 individuals) discordant for IBD (CD: 15, UC: 16). 15/32 twin pairs were monozygotic, 43/62 of participants were female, the median age was 47 years (interquartile range: 34–58.5). Of 31 participants with IBD, 7 had signs of active inflammation based on endoscopy, Harvey–Bradshaw index or short clinical colitis activity index. Differences (log-linear discriminant analysis score >3) in the microbial composition of IgA-coated bacteria were observed between CD patients and their twin-siblings not affected by IBD: Dorea formicigenerans (increased in IgA coating), Parabacteroides sp., Christensenellaceae sp., Clostridium sp. and Mollicutes RF39 sp. (decreased in IgA coating). In ulcerative colitis patients, an increase in IgA-coating was observed for Ruminococcus gnavus and Dorea formicigenerans, while Turicibacter sp., Barnesiellaceae sp. and an unclassified Clostridiales sp. were decreased in IgA-coating compared with their twin-siblings not affected by IBD. Conclusion In twins affected by IBD, the pattern of IgA-coated bacteria differs between IBD and non-IBD affected individuals. These data on immune-bacteria interactions could serve as a starting point for the elucidation of the immune-responses triggered by specific bacteria in IBD.


Author(s):  
Frederick Vogel ◽  
Martin Reincke

AbstractPatients with endogenous or exogenous glucocorticoid (GC) excess exhibit a range of side effects, including an increased risk of infections. Via both mechanism, immune impairments and cardiometabolic concomitant diseases, patients with GC excess could be at increased risk for COVID-19. The impact on incidence and outcome of a SARS-CoV-2 infection in this population are not yet completely clear. This review aims to compile the data available to date and to discuss the existing literature on this topic. Further we highlight potential effects of SARS-CoV-2 on the hypothalamic-pituitary-adrenal axis as well as the influence of endogenous or exogenous GC excess on SARS-CoV-2 mRNA vaccination. There is growing evidence suggesting an increased risk of infection and severe outcome in patients with high-dose GC therapy after contracting SARS-CoV-2. The few data and case reports on patients with endogenous GC excess and SARS-CoV-2 infection point in a similar direction: chronic GC excess seems to be associated with an unfavorable course of COVID-19. Whether this is mainly a primary immune-mediated effect, or also triggered by the many GC-associated comorbidities in this population, is not yet fully understood. Patients with endogenous or exogenous GC excess should be considered as a vulnerable group during the SARS-CoV-2 pandemic. Regardless of the cause, vaccination and consistent surveillance and control of associated comorbidities are recommended.


2019 ◽  
Vol 10 (1) ◽  
pp. 27-32 ◽  
Author(s):  
A.C. Wing ◽  
M. Kremenchutzky

Gut microbiome interaction goes beyond commensal function as vitamin production or support nutrients digestion. It also interplays with the host immune system and may be related to the development of immune-mediated diseases. Multiple sclerosis patients have dysbiosis compared to healthy individuals. But how this relates to disease development and severity is still uncertain. Dietary change including probiotic mixtures or ketogenic regimen has proven to change microbiome in multiple sclerosis (MS) subjects to one similar to healthy controls. However, proof of clinical benefits is lacking. We dissert on current knowledge about immune system and gut bacteria interactions. We discuss faecal microbial transplantation as a potential intervention to ameliorate gut dysbiosis in MS as well as the caveats of a clinical trial design.


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