Premium
Aqueous fraction of Sauropus androgynus might be responsible for bronchiolitis obliterans
Author(s) -
HASHIMOTO IZUMI,
IMAIZUMI KAZUYOSHI,
HASHIMOTO NAOZUMI,
FURUKAWA HIROSHI,
NODA YUKIHIRO,
KAWABE TSUTOMU,
HONDA TOYOHIRO,
OGAWA TOMOMI,
MATSUO MASAKI,
IMAI NAOYUKI,
ITO SATORU,
SATO MITSUO,
KONDO MASASHI,
SHIMOKATA KAORU,
HASEGAWA YOSHINORI
Publication year - 2013
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/j.1440-1843.2012.02286.x
Subject(s) - pathogenesis , cytokine , medicine , haematopoiesis , immunology , tumor necrosis factor alpha , fibrosis , chemokine , stromal vascular fraction , apoptosis , biology , stromal cell , cancer research , inflammation , pathology , stem cell , microbiology and biotechnology , biochemistry
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.