Role of intracellular zinc in molecular and cellular function in allergic inflammatory diseases.

gnorimies20.15 shared this article with you from Inoreader Role of intracellular zinc in molecular and cellular function in allergic inflammatory diseases. Via Head and Neck Related Articles Role of intracellular zinc in molecular and cellular function in allergic inflammatory diseases. Allergol Int. 2020 Oct 27;: Authors: Suzuki M, Suzuki T, Watanabe M, Hatakeyama S, Kimura S, Nakazono A, Honma A, Nakamaru Y, Vreugde S, Homma A Abstract Zinc is an essential micronutrient in human body and a vital cofactor for the function of numerous proteins encoded by the human genome. Zinc has a critical role in maintaining many biochemical and physiological processes at the molecular, cellular, and multiple organ and systemic levels. The alteration of zinc homeostasis causes dysfunction of many organs and systems. In the immune system, zinc regulates the differentiation, proliferation and function of inflammatory cells, including T cells, eosinophils, and B cells, by modifying several signaling pathways such as NFκB signaling pathways and TCR signals. An adequate zinc level is essential for proper immune responses and decreased zinc levels were reported in many allergic inflammatory diseases, including atopic dermatitis, bronchial asthma, and chronic rhinosinusitis. Decreased zinc levels often enhance inflammatory activation. On the other hand, the inflammatory conditions alter the intracellular homeostasis of zinc, oft en decreasing zinc levels. These findings implied that there could be a vicious cycle between zinc deficiency and inflammatory conditions. In this review, we present recent evidence on the involvement of zinc in atopic dermatitis, bronchial asthma, and chronic rhinosinusitis, with insights into the involvement of zinc in the underlying molecular and cellular mechanisms related to these allergic inflammatory diseases. PMID: 33127267 [PubMed - as supplied by publisher] View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.