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A Carbon Nanotube Toxicity Paradigm Driven by Mast Cells and the IL‐33/ST2 Axis
Author(s) -
Katwa Pranita,
Wang Xiaojia,
Urankar Rakhee N.,
Podila Ramakrishna,
Hilderbrand Susana C.,
Fick Robert B.,
Rao Apparao M.,
Ke Pu Chun,
Wingard Christopher J.,
Brown Jared M.
Publication year - 2012
Publication title -
small
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.785
H-Index - 236
eISSN - 1613-6829
pISSN - 1613-6810
DOI - 10.1002/smll.201200873
Subject(s) - carbon nanotube , interleukin 33 , nanotechnology , mast (botany) , toxicity , mast cell , materials science , chemistry , interleukin , cytokine , medicine , immunology , organic chemistry
Concern about the use of nanomaterials has increased significantly in recent years due to potentially hazardous impacts on human health. Mast cells are critical for innate and adaptive immune responses, often modulating allergic and pathogenic conditions. Mast cells are well known to act in response to danger signals through a variety of receptors and pathways including IL‐33 and the IL‐1‐like receptor ST2. Here, the involvement of mast cells and the IL‐33/ST2 axis in pulmonary and cardiovascular responses to multi‐walled carbon nanotube (MWCNT) exposure are examined. Toxicological effects of MWCNTs are observed only in mice with a sufficient population of mast cells and are not observed when mast cells are absent or incapable of responding to IL‐33. Our findings establish for the first time that mast cells and the IL‐33/ST2 axis orchestrates adverse pulmonary and cardiovascular responses to an engineered nanomaterial, giving insight into a previously unknown mechanism of toxicity. This novel mechanism of toxicity could be used for assessing the safety of engineered nanomaterials and provides a realistic therapeutic target for potential nanoparticle induced toxicities.