Carbon nanotubes can activate immune cells, leading to increased lung inflammation and fibrosis through the release of pro-inflammatory mediators.
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A variety of production and applications of carbon nanotubes (CNTs) lead to an increased risk of lung inflammation and fibrosis. Pulmonary immune cells play a vital role in protecting the delicate structures of gaseous exchange against invasion from nanoparticles. Accumulating studies demonstrate a close relationship between immune cells and lung injury by CNTs. CNTs can directly or indirectly activate immune cells to accelerate the release of pro-inflammatory and pro-fibrotic mediators via various signaling pathways. Immune cell-regulated lung tissue injury, in combination with inflammatory response, dysregulated wound repair, and fibroblast proliferation, leads to ongoing tissue remodeling and formation of fibrotic foci seen in end-stage pulmonary fibrosis. Therefore, more insight is needed to integrate basic immune mechanisms into translational research and finally new therapies of CNTs-induced respiratory toxicity. In this article, functional alterations of immune cells, including neutrophils, monocytes, macrophages, T cells, etc., that are implicated in the initiation and progression of inflammation and fibrosis in CNTs-exposed lungs are summarized and discussed by databases searched (e.g. PubMed, Scopus and Web of Science) and the inclusive dates of the search (up to 2025). This review would provide comprehensive insights into the mechanistic understanding of lung inflammation and fibrosis induced by CNTs.
Zhang et al. (Fri,) reported a other. Carbon nanotubes can activate immune cells, leading to increased lung inflammation and fibrosis through the release of pro-inflammatory mediators.