ABSTRACT
The current treatment and prevention procedures of oral disorders follow a very targeted approach considering mouth and its structures as a system that is completely independent, than the rest of the body. The main therapeutic approach is to keep the levels of oral bacteria and hygiene in an acceptable range compatible with oral-mouth health, completely separated from systemic microbial homeostasis (eubiosis vs dysbiosis). This can negatively impact the diagnosis of a more complex systemic disease and its progression. Dysbiosis occurs as a consequence of imbalance in oral and gut microbiota which leads to cardiovascular diseases, diabetes mellitus, rheumatoid arthritis, and Alzheimer's disease, as reported in current literature. Likewise, there is a need to highlight and develop a novel philosophical approach in the treatments for oral diseases that will necessarily involve nonconventional approaches.
Subject(s)
Dysbiosis/microbiology , Endocrine System Diseases/microbiology , Gastrointestinal Microbiome , Immune System Diseases/microbiology , Metabolic Diseases/microbiology , Mouth Mucosa/microbiology , Animals , Dysbiosis/therapy , Endocrine System Diseases/therapy , Fatty Acids/administration & dosage , Fatty Acids/adverse effects , Gastrointestinal Microbiome/drug effects , Gastrointestinal Microbiome/physiology , Gastrointestinal Tract , Humans , Immune System Diseases/therapy , Metabolic Diseases/therapy , Microbiota/drug effects , Microbiota/physiology , Mouth Mucosa/physiology , Probiotics/administration & dosageABSTRACT
Type 1 diabetes (T1D) and Hashimoto's thyroiditis (HT) are the two most common autoimmune endocrine diseases that have rising global incidence. These diseases are caused by the immune-mediated destruction of hormone-producing endocrine cells, pancreatic beta cells and thyroid follicular cells, respectively. Both genetic predisposition and environmental factors govern the onset of T1D and HT. Recent evidence strongly suggests that the intestinal microbiota plays a role in accelerating or preventing disease progression depending on the compositional and functional profile of the gut bacterial communities. Accumulating evidence points towards the interplay between the disruption of gut microbial homeostasis (dysbiosis) and the breakdown of host immune tolerance at the onset of both diseases. In this review, we will summarize the major recent findings about the microbiome alterations associated with T1D and HT, and the connection of these changes to disease states. Furthermore, we will discuss the potential mechanisms by which gut microbial dysbiosis modulates the course of the disease, including disruption of intestinal barrier integrity and microbial production of immunomodulatory metabolites. The aim of this review is to provide broad insight into the role of gut microbiome in the pathophysiology of these diseases.
Subject(s)
Endocrine System Diseases/metabolism , Gastrointestinal Microbiome , Autoimmune Diseases/immunology , Autoimmune Diseases/microbiology , Bile Acids and Salts/metabolism , Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 1/microbiology , Disease Progression , Dysbiosis/immunology , Dysbiosis/microbiology , Endocrine System Diseases/immunology , Endocrine System Diseases/microbiology , Fatty Acids, Volatile/metabolism , Genetic Predisposition to Disease , Hashimoto Disease/immunology , Hashimoto Disease/microbiology , Homeostasis , Humans , Incidence , PermeabilityABSTRACT
Human microbiota seems to play a key role in endocrine and reproductive systems. Fortunately, microbiota reproductive dysbiosis start to be treated by probiotics using typical species from genus Lactobacillus. This work presents the compiled and analysed results from the most up-to-date information from clinical trials regarding microbiota, fertility, probiotics and oral route administration, reviewing open access scientific documents. These studies analyse the clinical impact of probiotics administered on several endocrine disorders' manifestations in women: mastitis; vaginal dysbiosis; pregnancy complication disorders; and polycystic ovary syndrome. In all cases, the clinical modulation achieved by probiotics was evaluated positively through the improvement of specific disease outcomes with the exception of the pregnancy disorders studies, where the sample sizes results were statistically insufficient. High amounts of studies were discarded because no data were provided on specific probiotic strains, doses, impact on the individual autochthon microbiota, or data regarding specific hormonal values modifications and endocrine regulation effects. However, most of the selected studies with probiotics contained no protocolised administration. Therefore, we consider that intervention studies with probiotics might allocate the focus, not only in obtaining a final outcome, but in how to personalise the administration according to the disorder to be palliated.
Subject(s)
Dietary Supplements , Dysbiosis/therapy , Endocrine System Diseases/therapy , Infertility, Female/therapy , Probiotics/therapeutic use , Dysbiosis/complications , Endocrine System/microbiology , Endocrine System Diseases/microbiology , Female , Genitalia, Female/microbiology , Humans , Infertility, Female/microbiology , Microbiota , Pregnancy , Treatment OutcomeABSTRACT
Helicobacter pylori (H pylori) infection is a leading world-wide infectious disease as it affects more than half of the world population and causes chronic gastritis, peptic ulcer disease and gastric malignancies. The infection elicits a chronic cellular inflammatory response in the gastric mucosa. However, the effects of this local inflammation may not be confined solely to the digestive tract but may spread to involve extra-intestinal tissues and/or organs. Indeed, H pylori infection has been epidemiologically linked to extra-digestive conditions and diseases. In this context, it has been speculated that H pylori infection may be responsible for various endocrine disorders, such as autoimmune thyroid diseases, diabetes mellitus, dyslipidemia, obesity, osteoporosis and primary hyperparathyroidism. This is a review of the relationship between H pylori infection and these endocrine disorders.
Subject(s)
Endocrine System Diseases , Helicobacter Infections/physiopathology , Helicobacter pylori/metabolism , Diabetes Mellitus/microbiology , Diabetes Mellitus/physiopathology , Dyslipidemias/microbiology , Dyslipidemias/physiopathology , Endocrine System Diseases/microbiology , Endocrine System Diseases/physiopathology , Humans , Hyperparathyroidism/microbiology , Hyperparathyroidism/physiopathology , Obesity/microbiology , Obesity/physiopathology , Osteoporosis/microbiology , Osteoporosis/physiopathology , Thyroid Diseases/microbiology , Thyroid Diseases/physiopathologyABSTRACT
Sixty-two patients with cardiovascular, gastrointestinal, and endocrine diseases aged over 60 years and 27 healthy young people aged 16-18 years (controls) were examined in order to evaluate the qualitative composition and dissemination of oral microflora in elderly people with general somatic diseases. Microbiological study revealed changes in the qualitative composition and dissemination of the oral mucosa microflora, which depended on patient's age, disease, and treatment administered for somatic disease.
Subject(s)
Mouth Mucosa/drug effects , Mouth Mucosa/microbiology , Adolescent , Age Factors , Aged , Bacterial Physiological Phenomena/drug effects , Cardiovascular Diseases/complications , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/microbiology , Digestive System Diseases/complications , Digestive System Diseases/drug therapy , Digestive System Diseases/microbiology , Endocrine System Diseases/complications , Endocrine System Diseases/drug therapy , Endocrine System Diseases/microbiology , Humans , Middle AgedABSTRACT
The literature examined in this review points to the possible involvement of infectious agents in the pathogenesis of autoimmune endocrine diseases, primarily autoimmune thyroid disease and diabetes mellitus. Various mechanisms have been proposed to explain induction of autoimmunity by infection but it seems that three possibilities may be important in individuals susceptible to developing autoimmune disease: molecular mimicry (perhaps to retroviruses); polyclonal T cell activation (by an endogenous superantigen or an infecting organism); and MHC class II antigen induction. It seems reasonable that all three mechanisms operate together or separately in different individuals. Data continue to accumulate in favour of infectious agents being important initiators of autoimmune disease.
Subject(s)
Autoimmune Diseases , Endocrine System Diseases/immunology , Infections , Animals , Autoantigens , Diabetes Mellitus/genetics , Diabetes Mellitus/immunology , Diabetes Mellitus/microbiology , Endocrine System Diseases/microbiology , Histocompatibility Antigens , Humans , Thyroid Diseases/immunology , Thyroid Diseases/microbiology , Virus DiseasesABSTRACT
Immune responses are initiated by HLA-DR+ cells, which present antigen to T cells. Observations that HLA-DR may be experimentally induced on thyroid epithelium and that HLA-DR occurs on thyrocytes in autoimmune thyroid diseases suggest a mechanism of autoimmunity with special relevance to organ-specific diseases. This involves the local aberrant expression of HLA-DR antigens by epithelial cells and their subsequent capacity to present autoantigens occurring on their surfaces to T lymphocytes. For autoantigens which T cells recognise infrequently because of their restricted tissue location and low concentration in the circulation, T-cell tolerance is unlikely, and so induction of autoreactive T cells would occur. Because interferon is the best known inducer of DR antigen expression and viral infections may predate endocrine autoimmunity, the following sequence seems likely: local viral infection which causes interferon production, or other local environmental factors which would induce DR expression, presentation of autoantigens, and subsequent autoimmune T-cell induction. These T cells would activate effector B and T cells. Whether the initial induction of autoimmune T cells leads to autoimmune disease would depend on factors such as abnormalities of the suppressor T-cell pathway, reported to coexist with autoimmunity and necessary to induce autoimmune disease in mice. This mechanism of autoimmune disease induction explains vague associations with viral infections and long latency periods before disease becomes manifest and gives a simple explanation for the well-documented association between HLA-DR and autoimmune diseases in man.
Subject(s)
Autoimmune Diseases/immunology , Endocrine System Diseases/immunology , Genes, MHC Class II , Histocompatibility Antigens Class II/immunology , Autoantigens/genetics , Autoantigens/immunology , Autoimmune Diseases/genetics , Autoimmune Diseases/microbiology , Endocrine Glands/immunology , Endocrine System Diseases/genetics , Endocrine System Diseases/microbiology , HLA-DR Antigens , Humans , Immune Tolerance , Models, Biological , Organ Specificity , T-Lymphocytes/immunology , Thyroid Gland/immunology , Virus Diseases/immunologySubject(s)
Autoantibodies/analysis , Diabetes Mellitus/immunology , Endocrine System Diseases/immunology , Rubella/congenital , Child , Child, Preschool , Diabetes Mellitus/microbiology , Endocrine System Diseases/microbiology , Female , Humans , Infant , Infant, Newborn , Islets of Langerhans/immunology , Rubella/immunology , Syndrome , Thyroid Gland/immunologySubject(s)
Candida/isolation & purification , Disease , Mouth/microbiology , Adult , Brain Diseases/microbiology , Cardiovascular Diseases/microbiology , Endocrine System Diseases/microbiology , Eye Diseases/microbiology , Female , Gastrointestinal Diseases/microbiology , Hematologic Diseases/microbiology , Humans , Hypersensitivity/microbiology , Inflammation/microbiology , Male , Neoplasms/microbiology , Nervous System Diseases/microbiology , Otorhinolaryngologic Diseases/microbiology , Pregnancy , Pregnancy Complications/microbiology , Respiratory Tract Diseases/microbiology , Tuberculosis, Pulmonary/microbiology , Urologic Diseases/microbiology , Wounds and Injuries/microbiologyABSTRACT
Both male and female pigs given a ration containing corn invaded by Fusarium roseum, in amounts sufficient to provide 500 to 600 ppm of F-2, for the first 64 days of the test and which for another 60 days were given a commercial pig ration were much lower in weight than the controls which were given a commercial pig ration throughout. In relation to the weight of the animals, in the pigs receiving the ration containing F-2, the weight of the uterine horn of the gilts was much greater and the weight of the testes of the males was much less than the weight of the same organs of the controls.