| Wu CH |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=2 ------>paper_class2=1 ------>vol=155 ------>confirm_bywho=shiemin ------>insert_bywho=weipinho ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=545 ------>medlineContent= ------>unit=E0116 ------>insert_date=20050221 ------>iam=4 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN=None ------>authors_c=None ------>score=500 ------>journal_name=The Journal of TRAUMA_ Injury, Infection, and Critical Care ------>paper_name=Nitric Oxide Modulates Pro- and Anti-inflammatory Cytokines in Lipopolysaccharide-Activated Macrophages ------>confirm_date=20050507 ------>tch_id=086025 ------>pmid=14501900 ------>page1=540 ------>fullAbstract=BACKGROUND: Sepsis is a serious and life-threatening syndrome that occurs in intensive care unit patients. Lipopolysaccharide (LPS) has been implicated as one of major causes of sepsis. Nitric oxide (NO) and cytokines are involved in sepsis-induced inflammatory responses. This study is aimed at evaluating the effects of NO on the modulation of pro- and anti-inflammatory cytokines in LPS-activated macrophages and its possible mechanism. METHODS: N-Monomethyl arginine (NMMA), an inhibitor of NO synthase, was used in this study to suppress NO production. Mouse macrophage-like Raw 264.7 cells were exposed to LPS, NMMA, or a combination of NMMA and LPS. Cell viability was determined by the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-di-phenyltetrazolium bromide assay. The amounts of nitrite, an oxidative product of NO, in the culture medium were quantified according to the Griess reaction method. Enzyme-linked immunosorbent assay and reverse-transcriptase polymerase chain reaction were carried out to determine the expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-10 in macrophages. RESULTS: Exposure of macrophages to LPS, NMMA, and a combination of NMMA and LPS for 24 hours did not affect cell viability. LPS significantly increased the amounts of nitrite in macrophages (p < 0.01). Treatment with NMMA decreased LPS-enhanced nitrite (p < 0.01) in a concentration-dependent manner. Analyses of enzyme-linked immunosorbent assays and reverse-transcriptase polymerase chain reaction revealed that LPS significantly induced TNF-alpha, IL-1 beta, and IL-10 proteins and mRNA (p < 0.01). A combined treatment with NMMA and LPS significantly blocked LPS-induced TNF-alpha and IL-1 beta (p < 0.01), but synergistically enhanced LPS-induced IL-10 (p < 0.05) protein and RNA. CONCLUSION: This study has shown that NO suppression can inhibit LPS-induced TNF-alpha and IL-1 beta but enhance IL-10, and the modulation occurs at a pretranslational level. ------>tmu_sno=None ------>sno=10495 ------>authors2=Chen TL ------>authors3=Chen TG ------>authors4=Ho WP ------>authors5=Chiu WT ------>authors6=Chen RM ------>authors6_c=None ------>authors=Wu CH ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Nitric oxide modulates pro- and anti-inflammatory cytokines in lipopolysaccharide-activated macrophages. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no=3 ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2003 ------>submit_flag=None ------>publish_month=None |