Extreme temperatures and the epithelial barrier theory.
5 affiliations
- 1Swiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Herman Burchard Str. 9, Davos, CH-7265 , Switzerland.
- 2Department of Biochemistry and Molecular Biology, School of Chemistry, Complutense University of Madrid, Madrid, Spain.
- 3Department of Genetics, Faculty of Veterinary Medicine, Bursa Uludag University, Bursa, Turkey.
- 4Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
- 5Swiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Herman Burchard Str. 9, Davos, CH-7265 , Switzerland. [email protected].
Abstract
Extreme temperatures are now recognized as significant global health threats, driving morbidity and mortality across diverse diseases by compromising epithelial barrier integrity and causing periepithelial inflammation. The epithelial barrier theory posits that environmentally induced barrier dysfunction, driven by modern industrial and urban exposures, leads to compromised surfaces of the exposed tissues accompanied by epithelial activation and barrier dysfunction, microbial dysbiosis, loss of commensal bacteria, opportunistic pathogen colonization, bacterial translocation, inflammation and immune dysregulation. While toxic chemical exposures have been the primary focus of barrier research, temperature extremes-now intensified by anthropogenic warming, altered weather patterns and regional climatic variability-may similarly disrupt epithelial structure and function. Heat and cold can alter tight-junction regulation, induce mitochondrial and endoplasmic reticulum stress, oxidative stress, apoptosis and modify cytokine and chemokine profiles, thereby weakening barrier defenses and enhancing susceptibility to pollutants, allergens and pathogens. These effects may be amplified by co-exposures such as humidity fluctuations, UV radiation, wildfire smoke and increased pollutant loads associated with floods, droughts and other environmental catastrophes. Shifts in the exposome, including contamination of water systems and food chains, further link temperature-related barrier injury to rising rates of noncommunicable diseases (NCDs). Clinical and epidemiological evidence supports associations between heat waves and disease exacerbations, between cold exposure and infectious or allergic responses, and between altered weather patterns and growing prevalence of NCDs. This review synthesizes mechanistic, environmental and epidemiological data to highlight extreme temperatures as critical drivers of epithelial barrier dysfunction and global disease burden.
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BibTeX
@article{ogulur2026extreme,
title = {{Extreme temperatures and the epithelial barrier theory.}},
author = {Ismail Ogulur and Huseyn Babayev and Can Zeyneloglu and Bingjie Zhao and Ceren Bicer and Xiaoqing Liu and Yanni Zhang and Paolo D'Avino and Manru Li and Angel Maldonado and Jennifer Hotie and Sena Ardicli and Yagiz Pat and Mübeccel Akdis and Kari C Nadeau and Cezmi A Akdis},
journal = {Seminars in immunopathology},
year = {2026},
month = oct,
doi = {10.1007/s00281-026-01087-8},
url = {https://europepmc.org/article/MED/42902042},
note = {CC BY},
}
RIS
TY - JOUR
TI - Extreme temperatures and the epithelial barrier theory.
AU - Ismail Ogulur
AU - Huseyn Babayev
AU - Can Zeyneloglu
AU - Bingjie Zhao
AU - Ceren Bicer
AU - Xiaoqing Liu
AU - Yanni Zhang
AU - Paolo D'Avino
AU - Manru Li
AU - Angel Maldonado
AU - Jennifer Hotie
AU - Sena Ardicli
AU - Yagiz Pat
AU - Mübeccel Akdis
AU - Kari C Nadeau
AU - Cezmi A Akdis
PY - 2026
DA - 2026/10/20
JO - Seminars in immunopathology
DO - 10.1007/s00281-026-01087-8
UR - https://europepmc.org/article/MED/42902042
AB - Extreme temperatures are now recognized as significant global health threats, driving morbidity and mortality across diverse diseases by compromising epithelial barrier integrity and causing periepithelial inflammation. The epithelial barrier theory posits that environmentally induced barrier dysfunction, driven by modern industrial and urban exposures, leads to compromised surfaces of the exposed tissues accompanied by epithelial activation and barrier dysfunction, microbial dysbiosis, loss of commensal bacteria, opportunistic pathogen colonization, bacterial translocation, inflammation and immune dysregulation. While toxic chemical exposures have been the primary focus of barrier research, temperature extremes-now intensified by anthropogenic warming, altered weather patterns and regional climatic variability-may similarly disrupt epithelial structure and function. Heat and cold can alter tight-junction regulation, induce mitochondrial and endoplasmic reticulum stress, oxidative stress, apoptosis and modify cytokine and chemokine profiles, thereby weakening barrier defenses and enhancing susceptibility to pollutants, allergens and pathogens. These effects may be amplified by co-exposures such as humidity fluctuations, UV radiation, wildfire smoke and increased pollutant loads associated with floods, droughts and other environmental catastrophes. Shifts in the exposome, including contamination of water systems and food chains, further link temperature-related barrier injury to rising rates of noncommunicable diseases (NCDs). Clinical and epidemiological evidence supports associations between heat waves and disease exacerbations, between cold exposure and infectious or allergic responses, and between altered weather patterns and growing prevalence of NCDs. This review synthesizes mechanistic, environmental and epidemiological data to highlight extreme temperatures as critical drivers of epithelial barrier dysfunction and global disease burden.
SN - 1863-2297
SN - 1863-2300
ER -