To investigate the significance of the SARS-associated coronavirus (SARS-CoV) antibody,detected by ELISA and indirect immunofluorescence assays (IFA) for the SARS-CoV Vero E6 cell lysates,in non-SARS subjects, 114 ser...To investigate the significance of the SARS-associated coronavirus (SARS-CoV) antibody,detected by ELISA and indirect immunofluorescence assays (IFA) for the SARS-CoV Vero E6 cell lysates,in non-SARS subjects, 114 serum samples from healthy controls and 104 serum specimens from autoimmune disease patients were collected.The results of ELISA showed that among 114 sera from healthy controls,4 (3.5%) were positive of SARS-CoV-IgG antibody and 114 (100%) were all negative of SARS-CoV-IgM antibody;the specificity of SARS-CoV-IgG antibody for SARS patients was 96.5%,but the specificity of both SARS-CoV-IgG and -IgM antibodies for SARS patients was 100%.In 58 cases with SLE,positive rates of SARS-CoV-IgG and -IgM antibodies were 32.8% (19/58) and 8.6% (5/58),respectively,in which 11 cases (19%) were positive of both SARS-CoV-IgG and -IgM antibodies;in 10 cases with SS,positive rate of both SARS-CoV-IgG and -IgM antibodies was 10% (1/10);in 16 cases with MCTD,positive rate of SARS-CoV-IgG was 37.5% (6/16),positive rate of both SARS-CoV-IgG and -IgM antibodies was 6.3% (1/16);in 20 cases with RA,one case was positive (5%) of SARS-CoV-IgG.However,of all samples with positive SARS-CoV-IgG and -IgM antibodies for autoimmune diseases and healthy controls,SARS-CoV RNA and antibodies were all negative by RT-PCR and IFA.All sera for negative or positive ELISA results were also negative or positive results using ELISA with Vero E6 cells lysates.These studies showed that SARS-CoV Vero E6 cell lysates for the ELISA to detect SARS-CoV antibodies could lead to the false-positive reactions or cross-reactions of SARS-CoV antibodies in non-SARS diseases and healthy controls,and the false-positive reactions or cross-reactions were related to Vero E6 cell lysates and autoantibodies in non-SARS population.Cellular & Molecular Immunology.2004;1(4): 304-307.展开更多
Cigarette smoking is the top environmental risk factor for lung cancer. Nicotine, the addictive component of cigarettes, induces lung cancer cell proliferation, invasion and migration via the activation of nicotinic a...Cigarette smoking is the top environmental risk factor for lung cancer. Nicotine, the addictive component of cigarettes, induces lung cancer cell proliferation, invasion and migration via the activation of nicotinic acetylcholine receptors （nAChRs）. Genome-wide association studies （GWAS） show that CI4RNA5 gene encoding α5-nAChR is especially relevant to lung cancer. However, the mechanism of this subunit in lung cancer is not clear. In the present study, we demonstrate that the expression of α5-nAChR is correlated with phosphorylated STAT3 （pSTAT3） expression, smoking history and lower survival of non-small cell lung cancer （NSCLC） samples. Nicotine increased the levels of α5-nAChR mRNA and protein in NSCLC cell lines and activated the ]AK2/STAT3 signaling cascade. Nicotine-induced activation of JAK2/STAT3 signaling was inhibited by the silencing of α5-nAChR. Characterization of the CHRNA5 promoter revealed four STAT3-response elements. ChiP assays confirmed that the CHRNA5 promoter contains STAT3 binding sites. By silencing STAT3 expression, nicotine-induced upregulation of α5-nAChR was suppressed. Downregulation of α5-nAChR and/or STAT3 expression inhibited nicotine-induced lung cancer cell proliferation. These results suggest that there is a feedback loop between α5-nAChR and STAT3 that contributes to the nicotine-induced tumor cell proliferation, which indicates that α5-nAChR is an important therapeutic target involved in tobacco-associated lung carcinogenesis.展开更多
文摘To investigate the significance of the SARS-associated coronavirus (SARS-CoV) antibody,detected by ELISA and indirect immunofluorescence assays (IFA) for the SARS-CoV Vero E6 cell lysates,in non-SARS subjects, 114 serum samples from healthy controls and 104 serum specimens from autoimmune disease patients were collected.The results of ELISA showed that among 114 sera from healthy controls,4 (3.5%) were positive of SARS-CoV-IgG antibody and 114 (100%) were all negative of SARS-CoV-IgM antibody;the specificity of SARS-CoV-IgG antibody for SARS patients was 96.5%,but the specificity of both SARS-CoV-IgG and -IgM antibodies for SARS patients was 100%.In 58 cases with SLE,positive rates of SARS-CoV-IgG and -IgM antibodies were 32.8% (19/58) and 8.6% (5/58),respectively,in which 11 cases (19%) were positive of both SARS-CoV-IgG and -IgM antibodies;in 10 cases with SS,positive rate of both SARS-CoV-IgG and -IgM antibodies was 10% (1/10);in 16 cases with MCTD,positive rate of SARS-CoV-IgG was 37.5% (6/16),positive rate of both SARS-CoV-IgG and -IgM antibodies was 6.3% (1/16);in 20 cases with RA,one case was positive (5%) of SARS-CoV-IgG.However,of all samples with positive SARS-CoV-IgG and -IgM antibodies for autoimmune diseases and healthy controls,SARS-CoV RNA and antibodies were all negative by RT-PCR and IFA.All sera for negative or positive ELISA results were also negative or positive results using ELISA with Vero E6 cells lysates.These studies showed that SARS-CoV Vero E6 cell lysates for the ELISA to detect SARS-CoV antibodies could lead to the false-positive reactions or cross-reactions of SARS-CoV antibodies in non-SARS diseases and healthy controls,and the false-positive reactions or cross-reactions were related to Vero E6 cell lysates and autoantibodies in non-SARS population.Cellular & Molecular Immunology.2004;1(4): 304-307.
基金funded by grants from the National Natural Science Foundation of China(Nos.81272588,81602593,31671468 and 31672286)the Shandong Provincial Natural Science Foundation of China(No.ZR2012HM061)
文摘Cigarette smoking is the top environmental risk factor for lung cancer. Nicotine, the addictive component of cigarettes, induces lung cancer cell proliferation, invasion and migration via the activation of nicotinic acetylcholine receptors （nAChRs）. Genome-wide association studies （GWAS） show that CI4RNA5 gene encoding α5-nAChR is especially relevant to lung cancer. However, the mechanism of this subunit in lung cancer is not clear. In the present study, we demonstrate that the expression of α5-nAChR is correlated with phosphorylated STAT3 （pSTAT3） expression, smoking history and lower survival of non-small cell lung cancer （NSCLC） samples. Nicotine increased the levels of α5-nAChR mRNA and protein in NSCLC cell lines and activated the ]AK2/STAT3 signaling cascade. Nicotine-induced activation of JAK2/STAT3 signaling was inhibited by the silencing of α5-nAChR. Characterization of the CHRNA5 promoter revealed four STAT3-response elements. ChiP assays confirmed that the CHRNA5 promoter contains STAT3 binding sites. By silencing STAT3 expression, nicotine-induced upregulation of α5-nAChR was suppressed. Downregulation of α5-nAChR and/or STAT3 expression inhibited nicotine-induced lung cancer cell proliferation. These results suggest that there is a feedback loop between α5-nAChR and STAT3 that contributes to the nicotine-induced tumor cell proliferation, which indicates that α5-nAChR is an important therapeutic target involved in tobacco-associated lung carcinogenesis.
