Down-regulation of granulocyte-macrophage colony-stimulating factor by 3C-like proteinase in transfected A549 human lung carcinoma cells
Título
Down-regulation of granulocyte-macrophage colony-stimulating factor by 3C-like proteinase in transfected A549 human lung carcinoma cells
Autor
Tsai Hsien-Yu, Chen Miles, Wang Yao-Chen, Liao Hsien-Hua, Lin Johnson, Chen Shui-Tein, Tsay Gregory, Cheng Sun-Long
Descripción
Abstract Background Severe Acute Respiratory Syndrome (SARS) is a severe respiratory illness caused by a novel virus, the SARS coronavirus (SARS-CoV). 3C-like protease (3CLpro) of SARS-CoV plays a role in processing viral polypeptide precursors and is responsible of viral maturation. However, the function of 3CLpro in host cells remains unknown. This study investigated how the 3CLpro affected the secretion of cytokines in the gene-transfected cells. Results From immunofluorescence microscopy, the localization of c-myc tagged 3CLpro was detected both in the cytoplasm and nucleus of transfected A549 cells. Expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) was significantly decreased in 3CLpro-transfected cells by both RT-PCR and ELISA, but without changes in other cytokines, i.e., IL-1β, IL-6, IL-8, IL12p40, TNF-α, and TGF-β. Furthermore, the protein levels of NF-kB decreased in 3CLpro-transfected A549 cells when compared to EGFP transfected cells. Conclusions Our results suggest that the 3CLpro may suppress expression of GM-CSF in transfected A549 cells through down-regulation of NF-kB production.
Fecha
2011
Identificador
DOI: 10.1186/1471-2172-12-16
Fuente
BMC Immunology
Editor
BMC
Cobertura
Immunologic diseases. Allergy
Idioma
EN
Colección
Citación
Tsai Hsien-Yu, Chen Miles, Wang Yao-Chen, Liao Hsien-Hua, Lin Johnson, Chen Shui-Tein, Tsay Gregory, Cheng Sun-Long, “Down-regulation of granulocyte-macrophage colony-stimulating factor by 3C-like proteinase in transfected A549 human lung carcinoma cells,” SOCICT Open, consulta 18 de abril de 2026, https://www.socictopen.socict.org/items/show/1001.
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