Fundamental Toxicological Sciences

Paper Details

Fundamental Toxicological Sciences
Vol. 10 No. 1 February 17, 2023 p.27-30
mRNA expression profile of cytokines in rat primary alveolar macrophages treated with multiwalled carbon nanotube (MWCNT)
  • Katsumi Fukamachi (Department of Neurotoxicology, Nagoya City University Graduate School of Medical Sciences /
Nahida Sultana 1) , Katsumi Fukamachi 1) , Jiegou Xu 2) , Hiroyuki Tsuda 3) , Masumi Suzui 1)
1) Department of Neurotoxicology, Nagoya City University Graduate School of Medical Sciences , 2) Department of Immunology, School of Basic Medical Sciences, Anhui Medical University, China , 3) Nanotoxicology Project, Nagoya City University
Keywords: Carbon nanotube, Cytokine, Microarray, Macrophage

Multiwalled carbon nanotubes (MWCNT) are fiber-shaped nanomaterials that have a potential risk for cancer due to properties that are similar to asbestos. One type of nanotube called MWCNT-7 was categorized in Group 2B as possibly carcinogenic to humans by the International Agency for Research on Cancer. MWCNT-N, which is similar to MWCNT-7, is carcinogenic to the lung and pleura when administered to rats via the respiratory tract using intra-tracheal intra‐pulmonary spraying. Macrophages have an important role in the MWCNT induced pulmonary carcinogenicity. In this study, rat primary alveolar macrophages were employed to examine possible mechanism of carcinogenic effects of the MWCNT-N. MWCNT-N was fractionated into flow-through and retained fraction by passing it through a sieve with a pore size of 25 μm. Microarray analysis showed up-regulation of various cytokines in macrophages exposed to MWCNT-N. MWCNT-N strongly induced the expression of cytokines such as interleukin-6 (IL-6) in macrophages. In contrast, few cytokines were prominently down-regulated in macrophages treated with MWCNT-N. The sieve fractions did not have a significant effect on mRNA expression of cytokines in macrophages. These results provide useful information for understanding MWCNT-induced carcinogenicity via cytokine expression by macrophages.