| Ye YL |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=2 ------>paper_class2=1 ------>vol=19 ------>confirm_bywho=microbes ------>insert_bywho=yllee ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=84 ------>medlineContent= ------>unit=E0104 ------>insert_date=20040303 ------>iam=3 ------>update_date=None ------>author=??? ------>change_event=5 ------>ISSN=None ------>authors_c=None ------>score=446 ------>journal_name=Cytokine ------>paper_name=IL-12 inhibits eotaxin secretion of cultured primary lung cells and alleviates airway inflammation in vivo ------>confirm_date=20040507 ------>tch_id=092064 ------>pmid=12182842 ------>page1=76 ------>fullAbstract=The mechanisms that cause the inflammation of airway and lung tissue in asthma have been studied extensively. It is noted that type 1T helper cell (Th1)-related cytokines could decrease the accumulation of eosinophils in lung tissue and relieve airway constriction. But the therapeutic mechanisms of Th1 cytokines remain unclear. In this study, interleukin-12 (IL-12) DNA plasmid as a therapeutic reagent was delivered intravenously. Bronchoalveolar lavage (BAL) fluids were collected from IL-12 treated and control mice, and analyzed for cell composition and eotaxin level. The results showed that IL-12 DNA plasmid could effectively inhibit eosinophilia and airway inflammation in vivo. The level of eotaxin in BAL fluid also decreased. To further investigate the effect of Th1-related cytokines such as IL-12 or interferon-gamma (IFN-gamma) on the eotaxin level produced by lung cells, primary lung cell culture was established. The results demonstrated that both IL-12 and IFN-gamma could suppress eotaxin secretion from IL-13 or IL-4 stimulated primary lung cell culture. Moreover, the inhibitory effect of IL-12 could not be reversed by the administration of anti-IFN-gamma antibody. All the evidences suggested that IL-12 could regulate airway inflammation by suppressing the eotaxin secretion of lung tissue through an IFN-gamma independent mechanism. ------>tmu_sno=None ------>sno=8155 ------>authors2=Huang WC ------>authors3=Lee YL ------>authors4=Chiang BL ------>authors5= ------>authors6= ------>authors6_c=None ------>authors=Ye YL ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Interleukin-12 inhibits eotaxin secretion of cultured primary lung cells and alleviates airway inflammation in vivo. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2002 ------>submit_flag=None ------>publish_month=None |