{"refrec":{"BRefID":131648,"RR":"<b>Choi, H.S.; Yim, J.H.; Lee, H.K.; Pyo, S.</b> (2009). Immunomodulatory effects of polar lichens on the function of macrophages in vitro. <i>Mar. Biotechnol. 11(1)</i>: 90-98. <a href=\"https://dx.doi.org/10.1007/s10126-008-9121-x\" target=\"_blank\">https://dx.doi.org/10.1007/s10126-008-9121-x</a>","BEntID":125695,"PublicFlag":1,"CheckedFlag":1,"wosflag":1,"vabbflag":0,"RefStringPartII":". <i>Mar. Biotechnol. 11(1)</i>: 90-98. <a href=\"https://dx.doi.org/10.1007/s10126-008-9121-x\" target=\"_blank\">https://dx.doi.org/10.1007/s10126-008-9121-x</a>","DocTypID":8,"DocType":"Journal article","MarineFlag":1,"FreshFlag":0,"BrackishFlag":0,"TerrestrialFlag":0,"Authorstring":"Choi, H.S.; Yim, J.H.; Lee, H.K.; Pyo, S.","OrigTitleTranslFlag":0,"Authorstringtrunc":"Choi, H.S. <i>et al.</i>","Englishabstract":"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 <i>Caloplaca regalis</i> showed the highest nitric oxide (NO) production in murine peritoneal macrophages. Therefore, this study further examined the ability of <i>C. regalis</i> 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-α (TNF-α) and nitric oxide by macrophages. However, CR-ME had a little effect on the levels of reactive oxygen species, interleukin-1 and IFN-γ in CR-ME-treated macrophages. The CR-ME-induced tumoricidal activity was partially abrogated by a NO inhibitor and the anti-TNF-? antibody. Thus, the tumoricidal effect of CR-ME appeared to be mainly mediated by NO and TNF-α 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-κB transcription factor. Overall, these results indicate that the tumoricidal activity induced by CR-ME is mainly due to TNF-α and NO production, and the activation of macrophage by CR-ME is mediated probably via the p38 MAPK and NF-κB pathway. Our results may also provide some leads in the development of new immunomodulating drugs. 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