Abstract
Exposure to different organisms (bacteria, mold, virus, protozoan, helminths, among others) can induce epigenetic changes affecting the modulation of immune responses and consequently increasing the susceptibility to inflammatory diseases. Epigenomic regulatory features are highly affected during embryonic development and are responsible for the expression or repression of different genes associated with cell development and targeting/conducting immune responses. The well-known, “window of opportunity” that includes maternal and post-natal environmental exposures, which include maternal infections, microbiota, diet, drugs, and pollutant exposures are of fundamental importance to immune modulation and these events are almost always accompanied by epigenetic changes. Recently, it has been shown that these alterations could be involved in both risk and protection of allergic diseases through mechanisms, such as DNA methylation and histone modifications, which can enhance Th2 responses and maintain memory Th2 cells or decrease Treg cells differentiation. In addition, epigenetic changes may differ according to the microbial agent involved and may even influence different asthma or allergy phenotypes. In this review, we discuss how exposure to different organisms, including bacteria, viruses, and helminths can lead to epigenetic modulations and how this correlates with allergic diseases considering different genetic backgrounds of several ancestral populations.
Highlights
Asthma and allergy are the most common chronic inflammatory diseases, especially in children [1]
We present the concept of holobiont and discuss how exposure to different organisms, including bacteria, viruses, and helminths, can lead to epigenetic modulations and how this modulation correlates with allergic diseases, taking into account different genetic backgrounds of several ancestral populations
The epigenetic mechanisms are widespread in the different cell types of the human body, including cells that participate in an immune response pathway directly involved in the etiopathogenesis of asthma and other allergic diseases
Summary
Asthma and allergy are the most common chronic inflammatory diseases, especially in children [1]. Changes in the colonization of the lung microbiota of neonatal mice have [119, 120] been associated with decreased aeroallergen responsiveness induced by Helios– regulatory T cells (Helios– Treg cells) activated depending on interaction with programmed death-ligand 1 early in life, widely known as a regulator of allergic responses.
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