Environmental and genetic contribution in airway epithelial barrier in asthma pathogenesis.

Abstract

PURPOSE OF REVIEW:

To examine the recent, most relevant genetic and epigenetic modifications of the epithelial barrier in response to the environmental factors, including allergens, viruses, and pollutants, susceptible to participate to asthma.

RECENT FINDINGS:

IL-33 and TSLP gene polymorphisms are found in almost all asthma studies. Recent data have highlighted a new population of innate lymphoid cells, activated by these two cytokines, and mediating type 2 innate immunity dependent asthma. Gene variants of innate pattern recognition receptors associated with asthma have been evidenced in early viral infected high-risk birth cohorts, as well as polymorphisms in pathways involved in type I interferon (IFN) production, giving further insight into the role of viruses in asthma development. Novel epigenetic mechanisms have been evidenced in asthma and in response to the environmental pollutants, and point out genes like TSLP, which may link environmental pollution and asthma.

SUMMARY:

Genetic data support the role of a specific set of epithelial-derived proTh2 cytokines, including IL-33 and TSLP, as well as the role of decreased type I IFN in virus-induced impaired epithelial barrier. Epigenetic modifications of epithelial genes are promising mechanisms that warrant further investigation.

• Authors: Anne Tsicopoulos, Patricia de Nadai, Corine Glineur
• Journal: Current opinion in allergy and clinical immunology (Curr Opin Allergy Clin Immunol) Vol. 13 Issue 5 Pg. 495-9 (Oct 2013) ISSN: 1473-6322 [Electronic] United States
• PMID: 23945177 (Publication Type: Journal Article, Review)

Chemical References

• Allergens
• Cytokines
• IL33 protein, human
• Interferon Type I
• Interleukin-33
• Interleukins
• Receptors, Pattern Recognition
• Thymic Stromal Lymphopoietin

Topics

• Allergens (immunology)
• Animals
• Asthma (etiology, genetics)
• Cytokines (genetics)
• Environmental Exposure (adverse effects)
• Epigenesis, Genetic
• Gene-Environment Interaction
• Humans
• Immunity, Innate (genetics)
• Interferon Type I (immunology)
• Interleukin-33
• Interleukins (genetics)
• Polymorphism, Genetic
• Receptors, Pattern Recognition (genetics)
• Respiratory Mucosa (immunology)
• Th1-Th2 Balance
• Thymic Stromal Lymphopoietin