High-temperature calcined fullerene nanowhiskers as well as long needle-like multi-wall carbon nanotubes have abilities to induce NLRP3-mediated IL-1β secretion

Our plain-English summary of High-temperature calcined fullerene nanowhiskers as well as long needle-like multi-wall carbon nanotubes have abilities to induce NLRP3-mediated IL-1β secretion, by H. Cui, W. Wu, K. Okuhira, et al (Biochemical and Biophysical Research Communications, 2014).

The study

• Authors: H. Cui, W. Wu, K. Okuhira, K. Miyazawa, T. Hattori, K. Sai, M. Naito, K. Suzuki, T. Nishimura, Y. Sakamoto, A. Ogata, T. Maeno, A. Inomata, D. Nakae, A. Hirose, T. Nishimaki-Mogami
• Journal: Biochemical and Biophysical Research Communications
• Published: 2014;452(3):593-9
• Cited by: 13 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Because multi-wall carbon nanotubes (MWCNTs) have asbestos-like shape and size, concerns about their pathogenicity have been raised. Contaminated metals of MWCNTs may also be responsible for their toxicity. In this study, we employed high-temperature calcined fullerene nanowhiskers (HTCFNWs), which are needle-like nanofibers composed of amorphous carbon having similar sizes to MWCNTs but neither metal impurities nor tubular structures, and investigated their ability to induce production a major proinflammatory cytokine IL-1β via the Nod-like receptor pyrin domain containing 3 (NLRP3)-containing flammasome-mediated mechanism. When exposed to THP-1 macrophages, long-HTCFNW exhibited robust IL-1β production as long and needle-like MWCNTs did, but short-HTCFNW caused very small effect. IL-1β release induced by long-HTCFNW as well as by long, needle-like MWCNTs was abolished by a caspase-1 inhibitor or siRNA-knockdown of NLRP3, indicating that NLRP3-inflammasome-mediated IL-1β production by these carbon nanofibers. Our findings indicate that the needle-like shape and length, but neither metal impurities nor tubular structures of MWCNTs were critical to robust NLRP3 activation.

Copyright © 2014 Elsevier Inc. All rights reserved.

In plain English

This laboratory study, done in Japan, tested whether needle-shaped carbon fibers trigger an inflammatory signal in cultured human cells. The authors noted that multi-wall carbon nanotubes have an asbestos-like shape and size, but asbestos itself was not tested. They exposed a human macrophage-like cell line (THP-1) for 6 hours to three types of multi-wall carbon nanotubes and to long and short high-temperature calcined fullerene nanowhiskers. These are carbon fibers made by heating in vacuum that contain no metal impurities and are not tube-shaped. The long nanowhiskers caused robust, dose-dependent release of the inflammatory protein IL-1β, about 30% of the amount caused by one nanotube type (MWCNT-SD1) at the same concentration. The short nanowhiskers had a very small effect, although cells took up both lengths to a similar degree. IL-1β release caused by the long nanowhiskers and by two nanotube types was repressed by a caspase-1 inhibitor and diminished by silencing the NLRP3 gene. The authors concluded that needle-like shape and length, but neither metal impurities nor tubular structures, were critical to robust NLRP3 activation.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: In vitro laboratory experiment in a cultured human cell line
• Who was studied: THP-1 human macrophage-like cells obtained from the American Type Culture Collection, studied at laboratories in Tokyo, Japan; no people or animals were studied
• Exposure: Three vapor-grown multi-wall carbon nanotubes (MWCNT-M from Nanocarbon Technologies; MWCNT-SD1 and MWCNT-SD2 from Showa-Denko) and long (HTCFNW-L) and short (HTCFNW-S) high-temperature calcined fullerene nanowhiskers, made by heating fullerene nanowhiskers at 900 degrees C in vacuum. Cells were treated for 6 hours at stated concentrations in micrograms per mL of medium (for example 10 micrograms per mL). Asbestos was not tested.
• Main results:
  • Long nanowhiskers (HTCFNW-L) caused robust, dose-dependent IL-1β production, about 30% of that caused by MWCNT-SD1 at the same concentration
  • Short nanowhiskers (HTCFNW-S) had a very small but statistically significant effect that depended on the cells taking up the fibers
  • All three nanotube types increased IL-1β secretion with dose. For MWCNT-M and MWCNT-SD1 this was almost completely blocked by cytochalasin D, a drug that inhibits uptake of particles by cells.
  • In uptake measurements, MWCNT-SD1 and MWCNT-M increased the uptake signal. MWCNT-SD2, which was clumped (agglomerated), had no effect. Long and short nanowhiskers caused similar increases.
  • A caspase-1 inhibitor (zYVAD-fmk) completely inhibited IL-1β secretion induced by MWCNT-M and repressed release induced by MWCNT-SD1 and HTCFNW-L
  • Silencing the NLRP3 gene with three different siRNAs reduced IL-1β secretion induced by MWCNT-M, and diminished secretion induced by MWCNT-SD1 or HTCFNW-L
• The authors' conclusion: The authors concluded that the needle-like shape and length, but neither metal impurities nor the tube structure of multi-wall carbon nanotubes, were critical to robust NLRP3 activation

Topics

Medical terms in this study, explained in our Lexicon: Cytokine, Macrophage.

Related studies

• Long, needle-like carbon nanotubes and asbestos activate the NLRP3 inflammasome through a similar mechanism — J. Palomäki, E. Välimäki, et al. (2011)
• Gadolinium-based compounds induce NLRP3-dependent IL-1β production and peritoneal inflammation — C. Schmidt-Lauber, L. Bossaller, et al. (2015)
• PKC/ROS-Mediated NLRP3 Inflammasome Activation Is Attenuated by Leishmania Zinc-Metalloprotease during Infection — M.T. Shio, J.G. Christian, et al. (2015)
• Differential activation of the inflammasome in THP-1 cells exposed to chrysotile asbestos and Libby "six-mix" amphiboles and subsequent activation of BEAS-2B cells — M. Li, M.E. Gunter, et al. (2012)
• Double-walled carbon nanotubes trigger IL-1β release in human monocytes through Nlrp3 inflammasome activation — E. Meunier, A. Coste, et al. (2012)
• Nanoparticles activate the NLR pyrin domain containing 3 (Nlrp3) inflammasome and cause pulmonary inflammation through release of IL-1α and IL-1β — A.S. Yazdi, G. Guarda, et al. (2010)

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