Sly Saint
Senior Member (Voting Rights)
Cezmi A. Akdis
A steep increase in the prevalence of many chronic noncommunicable diseases occurred during the last 60 years, bringing them to a pandemic size.1 Our research and efforts to explain the reasons for this rise in their prevalence helped to develop the epithelial barrier hypothesis.
This hypothesis posits that disturbance of the epithelial barriers by laundry and dishwasher detergents, household cleaners, surfactants, enzymes and emulsifiers used in the food industry, cigarette smoke, particulate matter, diesel exhaust, ozone, nanoparticles, and microplastics cause tissue inflammation and microbial dysbiosis and play a role in many chronic noncommunicable diseases.1
The “epithelial barrier hypothesis” proposes mechanisms for the development of diseases of allergic, autoimmune, and neurodegenerative nature, with inflammation and tissue damage in the directly affected organs or distant organs that are not located directly at the skin and mucosal surfaces; accepts and embraces the hygiene and biodiversity hypotheses and links them to epithelial barrier defects and microbial dysbiosis; demonstrates possible ways of prevention of allergic and autoimmune diseases; and suggests future research directions.1
There is a need to support science and advance the understanding of the factors and molecular mechanisms associated with leaky epithelial barriers and inform policymakers of the detrimental effects of the potential causal or contributing substances. Here, I summarize the molecular and cellular mechanisms of the “epithelial barrier hypothesis” and supporting evidence.
A steep increase in the prevalence of many chronic noncommunicable diseases occurred during the last 60 years, bringing them to a pandemic size.1 Our research and efforts to explain the reasons for this rise in their prevalence helped to develop the epithelial barrier hypothesis.
This hypothesis posits that disturbance of the epithelial barriers by laundry and dishwasher detergents, household cleaners, surfactants, enzymes and emulsifiers used in the food industry, cigarette smoke, particulate matter, diesel exhaust, ozone, nanoparticles, and microplastics cause tissue inflammation and microbial dysbiosis and play a role in many chronic noncommunicable diseases.1
The “epithelial barrier hypothesis” proposes mechanisms for the development of diseases of allergic, autoimmune, and neurodegenerative nature, with inflammation and tissue damage in the directly affected organs or distant organs that are not located directly at the skin and mucosal surfaces; accepts and embraces the hygiene and biodiversity hypotheses and links them to epithelial barrier defects and microbial dysbiosis; demonstrates possible ways of prevention of allergic and autoimmune diseases; and suggests future research directions.1
There is a need to support science and advance the understanding of the factors and molecular mechanisms associated with leaky epithelial barriers and inform policymakers of the detrimental effects of the potential causal or contributing substances. Here, I summarize the molecular and cellular mechanisms of the “epithelial barrier hypothesis” and supporting evidence.
