Aqueous fraction of Sauropus androgynus might be responsible for bronchiolitis obliterans
Article first published online: 25 JAN 2013
© 2012 The Authors. Respirology © 2012 Asian Pacific Society of Respirology
Volume 18, Issue 2, pages 340–347, February 2013
How to Cite
HASHIMOTO, I., IMAIZUMI, K., HASHIMOTO, N., FURUKAWA, H., NODA, Y., KAWABE, T., HONDA, T., OGAWA, T., MATSUO, M., IMAI, N., ITO, S., SATO, M., KONDO, M., SHIMOKATA, K. and HASEGAWA, Y. (2013), Aqueous fraction of Sauropus androgynus might be responsible for bronchiolitis obliterans. Respirology, 18: 340–347. doi: 10.1111/j.1440-1843.2012.02286.x
- Issue published online: 25 JAN 2013
- Article first published online: 25 JAN 2013
- Accepted manuscript online: 15 OCT 2012 03:25AM EST
- Received 28 July 2011; invited to revise: 13 October 2011, 29 March, 22 July 2012; revised 23 November 2011, 26 May, 29 July 2012; accepted 12 August 2012 (Associate Editor: Yuben Moodley).
- constrictive bronchiolitis obliterans;
- murine bronchiolitis obliterans syndrome model;
- solvent system;
- tumour necrosis factor α
Background and objective: Bronchiolitis obliterans (BO) has been reported to develop following ingestion of Sauropus androgynus (SA), a leafy shrub distributed in Southeast Asia. Little is known about direct effects of SA on airway resident cells or haematopoietic cells in vitro. Identification of the SA component responsible for the development of BO would be an important key to elucidate its mechanism. We sought to elucidate the direct effects of SA on airway resident cells or haematopoietic cells and identify the SA element responsible for the pathogenesis of BO.
Methods: SA dry powder was partitioned into fractions by solvent extraction. Human and murine monocytic cells, epithelial cells and endothelial cells were cultured with SA solution or fractions eluted from SA. We also investigated the effect of SA in vivo using a murine BO syndrome (BOS) model.
Results: The aqueous fraction of SA induced significant increases of inflammatory cytokine and chemokine production from monocytic lineage cells. This fraction also induced significant apoptosis of endothelial cells and enhanced intraluminal obstructive fibrosis in allogeneic trachea allograft in the murine BOS model. We found individual differences in tumour necrosis factor α (TNF-α) production from monocytes of healthy controls stimulated by this aqueous fraction of SA, whereas it induced high-level TNF-α production from monocytes of patients with SA-induced BO.
Conclusions: These results suggest that an aqueous fraction of SA may be responsible for the pathogenesis of BO.