Nickel (Ni) is a chemical element that causes clinical manifestations such as allergic contact dermatitis (ACD) and systemic nickel allergy syndrome (SNAS), in nickel sensitized patients. ACD is the most common form of nickel allergy, due to contact with any objects containing nickel (buttons, jewellery, belt buckles etc.) in nickel sensitized patients The most common routes of exposure and sensitization to nickel are skin, and oral ingestion. The oral route represents not only a route of sensitization but also of tolerance; indeed it has been reported that exposure to nickel released from dental braces, before piercing, can reduce the appearance of nickel allergy. The human microbiome refers to collective genetic information of microorganisms that inhabit the body. These microorganisms, classified as beneficial (symbiotic) or dangerous (pathogenic), account for 90% of cells. They inhabit the gut predominantly and may be important in health or disease conditions such as obesity, irritable bowel syndrome (IBS) or atopic dermatitis (AD) so much so that they can be defined as the "second genome". Gastrointestinal microbiota variations may interrupt mucosal immunological tolerance, mainly through the gut microbiota, its metabolic products, dietary factors, epithelial cells, DCs, IgA antibodies, and regulatory T cells, leading to allergic conditions such as food allergy. Some studies reported that the introduction of nickel with a specific diet can induce changes in the equilibrium of the symbiotic intestinal microbiota. The role of Nickel sensitization and its influence on microbiota in patients with allergic and non-allergic diseases is still under investigation. Hereby we report on the microbiota changes in some allergic and non-allergic disorders where the role of nickel in diet has been taken into consideration. The knowledge of the impact of nickel on microbiota could play a role in possible and new therapeutic approaches.

Nickel sensitization influence on microbiota in allergic and non-allergic disorders: what's up?

L. Ricciardi
;
F. Furci;S. Gangemi
2021-01-01

Abstract

Nickel (Ni) is a chemical element that causes clinical manifestations such as allergic contact dermatitis (ACD) and systemic nickel allergy syndrome (SNAS), in nickel sensitized patients. ACD is the most common form of nickel allergy, due to contact with any objects containing nickel (buttons, jewellery, belt buckles etc.) in nickel sensitized patients The most common routes of exposure and sensitization to nickel are skin, and oral ingestion. The oral route represents not only a route of sensitization but also of tolerance; indeed it has been reported that exposure to nickel released from dental braces, before piercing, can reduce the appearance of nickel allergy. The human microbiome refers to collective genetic information of microorganisms that inhabit the body. These microorganisms, classified as beneficial (symbiotic) or dangerous (pathogenic), account for 90% of cells. They inhabit the gut predominantly and may be important in health or disease conditions such as obesity, irritable bowel syndrome (IBS) or atopic dermatitis (AD) so much so that they can be defined as the "second genome". Gastrointestinal microbiota variations may interrupt mucosal immunological tolerance, mainly through the gut microbiota, its metabolic products, dietary factors, epithelial cells, DCs, IgA antibodies, and regulatory T cells, leading to allergic conditions such as food allergy. Some studies reported that the introduction of nickel with a specific diet can induce changes in the equilibrium of the symbiotic intestinal microbiota. The role of Nickel sensitization and its influence on microbiota in patients with allergic and non-allergic diseases is still under investigation. Hereby we report on the microbiota changes in some allergic and non-allergic disorders where the role of nickel in diet has been taken into consideration. The knowledge of the impact of nickel on microbiota could play a role in possible and new therapeutic approaches.
2021
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3204433
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