Expression of Clara cell secretory protein in the lungs of rats exposed to silicon carbide whisker in vivo

Our plain-English summary of Expression of Clara cell secretory protein in the lungs of rats exposed to silicon carbide whisker in vivo, by Y. Morimoto, L. Ding, T. Oyabu, et al (Toxicology Letters, 2003).

The study

• Authors: Y. Morimoto, L. Ding, T. Oyabu, M. Hirohashi, H. Kim, A. Ogami, H. Yamato, I. Akiyama, H. Hori, T. Higashi, I. Tanaka
• Journal: Toxicology Letters
• Published: 2003;145(3):273-9
• Cited by: 6 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Intratracheal instillation studies have shown that exposure to silicon carbide whiskers (SiCW), an asbestos substitute, produces pulmonary fibrotic changes, suggesting that SiCW might have fibrogenic potential. It has been theorized that Clara cell secretory protein (CCSP) plays a critical role in regulating the acute inflammatory response in the lung. The present study was conducted to investigate the time course of the expression of CCSP in lungs exposed to SiCW in vivo. Male Wistar rats were administered 2 mg or 10 mg of SiCW suspended in saline by a single intratracheal instillation and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months of recovery time. The expression of CCSP was observed by reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot and immunostaining. Exposure to 10 mg of SiCW decreased in levels of CCSP mRNA at 3 days, 1 week, 1 month and 6 months following intratracheal instillation. The protein level of CCSP in SiCW-exposed rats was decreased at 1 day, 3 days and 1 month after a single instillation of 2 and 10 mg. These findings suggest that CCSP are involved not only in the acute injury but also in the chronic injury of the lung exposed to SiCW.

In plain English

In this animal experiment, the authors studied silicon carbide whiskers (SiCW), which the article describes as an asbestos substitute. Male Wistar rats received one dose of 2 mg or 10 mg of SiCW in saline, or saline alone, placed directly into the windpipe. There were five exposed and five control rats per group. The rats' lungs were examined 3 days, 1 week, 1 month, 3 months and 6 months later for a lung protein called Clara cell secretory protein (CCSP). CCSP gene activity was significantly lower than in controls at 3 days, 1 week, 1 month and 6 months in the 10 mg group, and only at 6 months in the 2 mg group. Neither dose lowered it at 3 months. CCSP protein was decreased at 3 days, 1 week and 1 month at both doses, was increased at 3 months in the 10 mg group, and was unchanged at 6 months. The authors wrote that these findings suggest CCSP is involved in both early and long-term lung injury from SiCW. The study was done in rats, not people.

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: Animal experiment: serial measurements in rats after a single intratracheal instillation (fluid placed directly into the windpipe)
• Who was studied: Male Wistar rats, 10 weeks old, bought from Kyudo (Kumamoto, Japan). Five exposed and five control rats for each exposure category.
• Exposure: A single intratracheal dose of 2 mg or 10 mg of silicon carbide whiskers in 0.4 ml saline; controls received saline. Geometric mean fiber diameter was 0.3 and geometric mean length was 5.1 (micrometres; the unit symbol is lost in the text). There were 1.63×10^8 fibers per mg, and 53% and 3.2% of fibers were longer than 5 and 20 micrometres respectively. Rats were followed for 3 days, 1 week, 1 month, 3 months and 6 months.
• Main results:
  • 2 mg SiCW group: CCSP gene activity (mRNA) in the lung was significantly lower than in controls at 6 months.
  • 10 mg SiCW group: CCSP mRNA was significantly lower than in controls at 3 days, 1 week, 1 month and 6 months.
  • At 3 months, neither the 2 mg nor the 10 mg dose decreased CCSP gene activity.
  • CCSP protein was decreased at 3 days, 1 week and 1 month in both the 2 mg and 10 mg groups.
  • At 3 months, CCSP protein was increased in the 10 mg group. The 2 mg group also showed an increase, but it was not statistically significant.
  • At 6 months, CCSP protein did not change in either dose group.
  • In the 10 mg group, CCSP staining of airway lining cells was weaker at 3 days.
  • Clara cell hyperplasia (an increase in the number of Clara cells) was often seen in SiCW-exposed lungs from 3 months after exposure, mainly in the distal airway.
• The authors' conclusion: The authors concluded that their findings suggest CCSP is involved in both the acute and the chronic injury of rat lungs exposed to SiCW.

Topics

Medical terms in this study, explained in our Lexicon: Fibrogenic.

Related studies

• Gene expression of surfactant protein-A and thyroid transcription factor-1 in lungs of rats exposed to silicon-carbide whisker in vivo — Y. Morimoto, L. Ding, et al. (2003)
• Pulmonary effects and biopersistence of deposited silicon carbide whisker after 1-year inhalation in rats — I. Akiyama, A. Ogami, et al. (2007)
• Histopathological changes in rat lung following intratracheal instillation of silicon carbide whiskers and potassium octatitanate whiskers — A. Ogami, Y. Morimoto, et al. (2007)
• Pulmonary response, in vivo, to silicon carbide whiskers — G.L. Vaughan, S.A. Trently, et al. (1993)
• In vitro activity of silicon carbide whiskers in comparison to other industrial fibers using four cell culture systems — N.F. Johnson, M.D. Hoover, et al. (1992)
• The carcinogenicity of WHO fibers of silicon carbide: SiC whiskers compared to cleavage fragments of granular SiC — K. Rödelsperger, B. Brückel (2006)

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