Abstracts of the 20th Congress of the International Federation of Associations of Anatomists
Year: 2022
Type: conference-abstract
Abstract: Humans are exposed to a variety of toxins and chemicals every day.According to the epithelial barrier hypothesis, exposure to many of these substances damages the epithelium, the thin layer of cells that covers the surface of our skin, lungs and intestine.A defective epithelial barrier has been demonstrated in allergic and autoimmune conditions such as asthma, atopic dermatitis, allergic rhinitis, chronic rhinosinusitis, eosinophilic esophagitis, celiac disease, and inflammatory bowel disease.In addition, leakiness of the gut epithelium is also implicated in systemic autoimmune and metabolic conditions such as diabetes, obesity, multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, and autoimmune hepatitis.Finally, distant inflammatory responses due to a 'leaky gut' and microbiome changes are suspected in Alzheimer's disease, Parkinson's disease, chronic depression and autism spectrum disorders.Here the "epithelial barrier hypothesis" is introduced, which proposes that the rise in epithelial barrier damaging agents linked to industrialization, urbanization and modern life underlies the rise in allergic, autoimmune and other chronic conditions.After breaking of the epithelial barriers by various environmental agents and infections, microbiome which normally floats above the skin and mucosas goes deeper between and beneath the epithelial barrier.Microbial dysbiosis and decreased biodiversity develop following the colonization of opportunistic pathogens, such as S. aureus, Moraxella, Haemophilus and Pneumococcus.An immune response and inflammation inside and beneath the epithelium develop with the aim of expulsion of dysbiotic microbiome, which is deeper than its usual anatomic position.Defective epithelial barrier healing capacity because of microbial dysbiosis, chronic tissue inflammation and epigenetic mechanisms lead to the chronicity of the disease.
DOI: 10.2399/ana.22.002s
Author: Nihal Apaydın
Institution: Ankara University
Language: English
Subfield: Dermatology
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W4313439343