UNIT 2 - DYSBIOSIS, ALLERGY AND AUTOIMMUNE DISEASE |
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Food Allergies and Dysbiosis
Autoimmune Disease and dysbiosis Article review Video review |
OBJECTIVES:
- Describe the connection of dysbiosis to food allergies.
- Discuss the role of dysbiosis to autoimmune diseases.
- Understand the nutritional consideration for gallstone disease.
- Neal Barnard, MD, (2009). Nutrition Guide for Clinicians.
- Michael Greger, MD, (2011). Nutrition Facts.
- Cleveland Clinic CME, (2018). Microbiome and Autoimmunity: What we need to know.
- Van der Meulen T.A., et al. Shared gut, but distinct oral microbiota composition in primary Sjogren’s syndrome and systemic lupus erythematosus. J. Autoimmun. 2018; 97: 77-87
Food Allergies and Dysbiosis
Food allergy is a clinical and public health problem defined as an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a food, immunoglobulin (Ig) E-mediated food allergy encompasses relatively immediate symptoms affecting the skin, respiratory, gastrointestinal, or cardiovascular systems. The cause of food allergy involves deviation from a default state of immune tolerance that is likely driven by antigen exposure, commensal microbiota, and their interactions. Resident microbial communities vastly outnumber human cells and genes, motivating interest in how their dysregulation (ie, dysbiosis) may influence host immunologic development and risk for allergic disorders. The sum of microbes, their genomic elements, and interactions in a given ecologic niche (ie, microbiome) differs by body site. Growing evidence supports a potential role for the gut microbiome in the pathogenesis and course of food allergy.
Early studies of gut microbiota and food allergy were culture-based, targeting groups of and individual bacteria of interest to explore hypotheses regarding the relationship between gut microbial characteristics and food allergy in early childhood. For example, a culture-based study of Spanish children with milk allergy showed that milk-allergic infants had higher total bacteria and anaerobic counts compared with healthy controls; after 6 months of differential formula intake, the 46 milk-allergic infants had higher proportions of lactobacilli and lower proportions of enterobacteria and bifidobacteria observed in bacterial cultures.
More recent studies of gut microbiota in food-allergic individuals have employed sequencing of the 16S rRNA gene, which encodes a component of the prokaryotic ribosome. Findings from 16S rRNA sequencing-based studies of food sensitization and food allergy defined broadly suggest that gut dysbiosis may precede the development of food allergy. Separately, a longitudinal study of 166 infants at ages 3 and 12 months from the Canadian Healthy Infant Longitudinal Development study showed that lower gut microbial richness at age 3 months was associated with increased likelihood of food sensitization by age 12 months. These associations between early gut microbiome composition and later food allergen sensitization or food allergy suggest a possible role for gut dysbiosis in the development of food allergy. The gut microbiome is known to change with time, with the most rapid change occurring in early life.
More recent studies of gut microbiota in food-allergic individuals have employed sequencing of the 16S rRNA gene, which encodes a component of the prokaryotic ribosome. Findings from 16S rRNA sequencing-based studies of food sensitization and food allergy defined broadly suggest that gut dysbiosis may precede the development of food allergy. Separately, a longitudinal study of 166 infants at ages 3 and 12 months from the Canadian Healthy Infant Longitudinal Development study showed that lower gut microbial richness at age 3 months was associated with increased likelihood of food sensitization by age 12 months. These associations between early gut microbiome composition and later food allergen sensitization or food allergy suggest a possible role for gut dysbiosis in the development of food allergy. The gut microbiome is known to change with time, with the most rapid change occurring in early life.
Knowledge about the gut microbiome’s role in food allergy is an emerging area with ample opportunities to deepen current foci as well as develop new directions. Because food allergy is a complex and heterogeneous disease, it is unlikely that the microbiota implicated in its pathogenesis and disease course, or even the microbiome in its entirety, can capture the interdependent dynamics of the molecular networks involved in food allergy. Our understanding of food allergy has been advanced not only by studies of the microbiome, but also by data generated through genome-wide association. Likely bacterial, viral, and fungal biomes interact with the human genome in complex ways to influence food allergy. System biology approaches have been used to examine relationships between microbiota and host genomic profiles in other disease areas such as inflammatory bowel disease.
Autoimmune disease and Dysbiosis
The pathogenesis of autoimmune diseases is not only attributed to genetic susceptibilities but also environmental factors, among which, disturbed gut microbiota has attracted increasing attention. Compositional and functional changes of gut microbiota have been reported in various autoimmune diseases, and increasing evidence suggests that disturbed gut microbiota contributes to their immunopathogenesis. The accepted mechanisms include abnormal microbial translocation, molecular mimicry, and dysregulation of both local and systemic immunity. Studies have also suggested microbiota-based classification models and therapeutic interventions for patients with autoimmune diseases. Further in-depth mechanistic studies on microbiota–autoimmunity interplay in autoimmune diseases are urgently needed and underway to explore novel and precise diagnostic biomarkers and develop disease and patient-tailored therapeutic strategies.
The commensal microbiota benefits from the continuous food supply, exogenous and endogenous, and constant physico-chemical conditions. Advantages for the host organism include metabolic, structural, protective, and other beneficial functions exerted by the commensal microbiota. The importance of commensal microbiota for the proper development and functioning of the host immune system is also well-recognized .
The commensal microbiota benefits from the continuous food supply, exogenous and endogenous, and constant physico-chemical conditions. Advantages for the host organism include metabolic, structural, protective, and other beneficial functions exerted by the commensal microbiota. The importance of commensal microbiota for the proper development and functioning of the host immune system is also well-recognized .
Presently, it is apparent that the microbiota and its products have a profound effect on the development and maintenance of the immune system. Germ-free animals, for example, have an impaired immune system that can be functionally restored after the inoculation of commensal bacteria. The extent of dependency of the immune system on commensals may even suggest the commensalocentric view. At the same time, not all commensals are alike. The dysbiotic populations, with no identifiable pathogens, can still confer the susceptibility to immune-mediated diseases.
The multiple animal models of human autoimmune diseases suggest the direct involvement of commensal microbiota in disease development. Under the germ-free conditions no disease is developing in the animal models of irritable bowel disease, rheumatoid arthritis and multiple sclerosis, supporting the notion of “no bugs, no disease,” while in some others they are only attenuated. In some models of the human autoimmune diseases causality is strengthened by the reintroduction of specific microorganisms restoring the disease severity.
Some members of the gut microbiota have been linked to autoimmune disease. Changing a single bacterial species and/or the entire commensal community can alter the outcome of a specific AD due to the imbalance of pathological/protective immune responses.
The multiple animal models of human autoimmune diseases suggest the direct involvement of commensal microbiota in disease development. Under the germ-free conditions no disease is developing in the animal models of irritable bowel disease, rheumatoid arthritis and multiple sclerosis, supporting the notion of “no bugs, no disease,” while in some others they are only attenuated. In some models of the human autoimmune diseases causality is strengthened by the reintroduction of specific microorganisms restoring the disease severity.
Some members of the gut microbiota have been linked to autoimmune disease. Changing a single bacterial species and/or the entire commensal community can alter the outcome of a specific AD due to the imbalance of pathological/protective immune responses.
Article Review
Diet Microbiota and Autoimmune Diseases
The influence of the microbiome on allergic sensitization to food
The influence of the microbiome on allergic sensitization to food
Video Review
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Unit Task
Submit your Reflective Journal after watching the videos, reading the lesson and article.