Engineered Nanomaterials and Type I Allergic Hypersensitivity Reactions.

Nasser B Alsaleh,Jared M Brown

doi:10.3389/fimmu.2020.00222

Abstract

Type I allergic hypersensitivity disorders (atopy) including asthma, atopic dermatitis, allergic rhinitis, and food allergy are on the rise in developed and developing countries. Engineered nanomaterials (ENMs) span a large spectrum of material compositions including carbonic, metals, polymers, lipid-based, proteins, and peptides and are being utilized in a wide range of industries including healthcare and pharmaceuticals, electronics, construction, and food industry, and yet, regulations for the use of ENMs in consumer products are largely lacking. Prior evidence has demonstrated the potential of ENMs to induce and/or aggravate type I allergic hypersensitivity responses. Furthermore, previous studies have shown that ENMs could directly interact with and activate key T-helper 2 (Th2) effector cell types (such as mast cells) and the complement system, which could result in pseudoallergic (non-IgE-mediated) hypersensitivity reactions. Nevertheless, the underlying molecular mechanisms of ENM-mediated induction and/or exacerbation of type I immune responses are poorly understood. In this review, we first highlight key examples of studies that have demonstrated inherent immunomodulatory properties of ENMs in the context of type I allergic hypersensitivity reactions, and most importantly, we attempt to put together the potential molecular mechanisms that could drive ENM-mediated stimulation and/or aggravation of type I allergic hypersensitivity responses.

Highlights

BackgroundThe immune system is the primary system for host protection against pathogens and foreign substance
We have previously demonstrated a role for the mast cell IL-33/ST2 axis in response to multiwalled carbon nanotubes (MWCNTs) toxicity [36]
Using mast cell-deficient and ST2−/− mouse models, we have demonstrated that MWCNT-induced adverse pulmonary and cardiovascular responses were almost completely abolished in the absence of mast cells or lack of expression of the mast cell ST2 receptors [36]

Summary

Introduction

BackgroundThe immune system is the primary system for host protection against pathogens and foreign substance. A growing body of research has demonstrated potential direct activation of the complement system and non-IgE mediated activation of effector immune cells including mast cells and basophils that could lead to type I hypersensitivities (Figure 2).

Results

Conclusion