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Immunomodulatory Effects of Polar Lichens on the Function of Macrophages In Vitro

Cited 11 time in scopus
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Title
Immunomodulatory Effects of Polar Lichens on the Function of Macrophages In Vitro
Other Titles
대식세포 기능에 있어 극지 지의류의 면역조절
Authors
Choi, Hye-Sook
Lee, Hong Kum
Pyo, Suhkneung
Yim, Joung Han
Subject
Biotechnology & Applied Microbiology; Marine & Freshwater Biology
Keywords
Antarctic; Caloplaca regalis; Immunomodulating activity; Macrophages; NF-κB
Issue Date
2009
Publisher
Springer
Citation
Choi, Hye-Sook, et al. 2009. "Immunomodulatory Effects of Polar Lichens on the Function of Macrophages In Vitro". MARINE BIOTECHNOLOGY, 11(1): 90-98.
Abstract
Lichen species were collected from King George Island (Antarctica) and were screened for their immunomodulatory effect. Among the lichens tested, the methanol extract (CR-ME) of Caloplaca regalis showed the highest nitric oxide (NO) production in murine peritoneal macrophages. Therefore, this study further examined the ability of C. regalis to induce secretory and cellular responses in macrophages. Macrophages were treated with various concentrations of CR-ME for 18 h. The CR-ME treatment induced tumoricidal activity and increased the production of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide by macrophages. However, CR-ME had a little effect on the levels of reactive oxygen species, interleukin-1 and IFN-gamma in CR-ME-treated macrophages. The CR-ME-induced tumoricidal activity was partially abrogated by a NO inhibitor and the anti-TNF-alpha antibody. Thus, the tumoricidal effect of CR-ME appeared to be mainly mediated by NO and TNF-alpha production from macrophages. Treating the macrophages with a p38 mitogen-activated protein kinase (MAPK) inhibitor partially blocked the tumoricidal activation induced by CR-ME, whereas inhibitors of the other kinases did not have an inhibitory effect. These results suggest that CR-ME induces the tumoricidal activity via the p38 MAPK-dependent pathway. Furthermore, electrophoretic mobility shift assay analyses revealed that the CR-ME treatment induced the activation of the NF-kappaB transcription factor. Overall, these results indicate that the tumoricidal activity induced by CR-ME is mainly due to TNF-alpha and NO production, and the activation of macrophage by CR-ME is mediated probably via the p38 MAPK and NF-kappaB pathway. Our results may also provide some leads in the development of new immunomodulating drugs.
URI
http://repository.kopri.re.kr/handle/201206/6038
DOI
http://dx.doi.org/10.1007/s10126-008-9121-x
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