Use of Polymeric Nanoparticle Platform Targeting the Liver To Induce Treg-Mediated Antigen-Specific Immune Tolerance in a Pulmonary Allergen Sensitization Model

Liu, Qi; Wang, Xiang; Liu, Xiangsheng; Kumar, Sanjan; Gochman, Grant E.; Ji, Ying; Liao, Yu‐Pei; Chang, Chong Hyun; Situ, Wesley; Lu, Jianqin; Jiang, Jinhong; Mei, Kuo‐Ching; Meng, Huan; Xia, Tian; Nel, André E.

doi:10.1021/acsnano.9b01444

Cited by 84 publications

(144 citation statements)

References 82 publications

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“…This ligand has been used to increase LSEC delivery by coating liposomes [266], lipid particles [267] and quantum dots [268]. Apolipoprotein B, or a part of its sequence, that is also a ligand for scavenger receptors stabilin-1 and 2 has been used to decorate nanoparticles [269,270] and liposomes [271]. Furthermore, the polymer poly(maleic anhydride-alt-1-octadecene) has also been used to coat superparamagnetic iron oxide nanoparticles in order to direct them to the sinusoidal endothelium [272].…”

Section: Lsec Targeting: Potential For Therapymentioning

confidence: 99%

The Endothelium as a Driver of Liver Fibrosis and Regeneration

Lafoz

Ruart

Anton

et al. 2020

Cells

103

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Liver fibrosis is a common feature of sustained liver injury and represents a major public health problem worldwide. Fibrosis is an active research field and discoveries in the last years have contributed to the development of new antifibrotic drugs, although none of them have been approved yet. Liver sinusoidal endothelial cells (LSEC) are highly specialized endothelial cells localized at the interface between the blood and other liver cell types. They lack a basement membrane and display open channels (fenestrae), making them exceptionally permeable. LSEC are the first cells affected by any kind of liver injury orchestrating the liver response to damage. LSEC govern the regenerative process initiation, but aberrant LSEC activation in chronic liver injury induces fibrosis. LSEC are also main players in fibrosis resolution. They maintain liver homeostasis and keep hepatic stellate cell and Kupffer cell quiescence. After sustained hepatic injury, they lose their phenotype and protective properties, promoting angiogenesis and vasoconstriction and contributing to inflammation and fibrosis. Therefore, improving LSEC phenotype is a promising strategy to prevent liver injury progression and complications. This review focuses on changes occurring in LSEC after liver injury and their consequences on fibrosis progression, liver regeneration, and resolution. Finally, a synopsis of the available strategies for LSEC-specific targeting is provided.

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Section: Lsec Targeting: Potential For Therapymentioning

confidence: 99%

The Endothelium as a Driver of Liver Fibrosis and Regeneration

Lafoz

Ruart

Anton

et al. 2020

Cells

103

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“…In both studies, sublingual AIT with PLGA NPs resulted in the eradication of allergic rhinitis symptoms and induced Th1/Treg responses. Liu et al (245) targeted liver sinusoidal endothelial cells with surface-modified PLGA NPs to induce tolerance against ovalbumin in a murine asthma model. In a murine cow's milk allergy model, prophylactic oral applications of beta-lactoglobulin-derived peptides incorporated into PLGA NPs induced tolerance to the whole whey protein after sensitization (242).…”

Section: Copolymer Nanoparticlesmentioning

confidence: 99%

Mechanisms of Particles in Sensitization, Effector Function and Therapy of Allergic Disease

et al. 2020

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Humans have always been in contact with natural airborne particles from many sources including biologic particulate matter (PM) which can exhibit allergenic properties. With industrialization, anthropogenic and combustion-derived particles have become a major fraction. Currently, an ever-growing number of diverse and innovative materials containing engineered nanoparticles (NPs) are being developed with great expectations in technology and medicine. Nanomaterials have entered everyday products including cosmetics, textiles, electronics, sports equipment, as well as food, and food packaging. As part of natural evolution humans have adapted to the exposure to particulate matter, aiming to protect the individual's integrity and health. At the respiratory barrier, complications can arise, when allergic sensitization and pulmonary diseases occur in response to particle exposure. Particulate matter in the form of plant pollen, dust mites feces, animal dander, but also aerosols arising from industrial processes in occupational settings including diverse mixtures thereof can exert such effects. This review article gives an overview of the allergic immune response and addresses specifically the mechanisms of particulates in the context of allergic sensitization, effector function and therapy. In regard of the first theme (i), an overview on exposure to particulates and the functionalities of the relevant immune cells involved in allergic sensitization as well as their interactions in innate and adaptive responses are described. As relevant for human disease, we aim to outline (ii) the potential effector mechanisms that lead to the aggravation of an ongoing immune deviation (such as asthma, chronic obstructive pulmonary disease, etc.) by inhaled particulates, including NPs. Even though adverse effects can be exerted by (nano)particles, leading to allergic sensitization, and the exacerbation of allergic symptoms, promising potential has been shown for their use in (iii) therapeutic approaches of allergic disease, for example as adjuvants. Hence, allergen-specific immunotherapy (AIT) is introduced and the role of adjuvants such as alum as well as the current understanding of their mechanisms of action is reviewed. Finally, future prospects of nanomedicines in allergy treatment are described, which involve modern platform technologies combining immunomodulatory effects at several (immuno-)functional levels.

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“…This could indeed open a new avenue in the treatment of hypersensitivity conditions such as type I allergic responses and autoimmune diseases (vs. only relieving the symptoms). For instance, it has been recently shown in a mouse model of ovalbumin-induced airway allergic disease that ovalbumin-loaded poly(lactic-co-glycolic acid) (PLGA) nanoparticles decorated with mannan (targeting mannose receptors) or ApoB (targeting scavenger receptors) for targeting liver sinusoidal endothelial cells were capable of stimulating Tregs resulting in systemic immune tolerance and alleviating disease outcomes (96). Therefore, ENMs should not always be negatively associated with allergic responses.…”

Section: Use Of Enms In Allergen Immunotherapymentioning

confidence: 99%

Engineered Nanomaterials and Type I Allergic Hypersensitivity Reactions

Alsaleh

Brown

2020

Front. Immunol.

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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.

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Use of Polymeric Nanoparticle Platform Targeting the Liver To Induce Treg-Mediated Antigen-Specific Immune Tolerance in a Pulmonary Allergen Sensitization Model

Cited by 84 publications

References 82 publications

The Endothelium as a Driver of Liver Fibrosis and Regeneration

The Endothelium as a Driver of Liver Fibrosis and Regeneration

Mechanisms of Particles in Sensitization, Effector Function and Therapy of Allergic Disease

Engineered Nanomaterials and Type I Allergic Hypersensitivity Reactions

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