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Updated: Apr 13, 2026

A 3D Human Lung Tissue Model for Functional Studies on Mycobacterium tuberculosis Infection
Published on: October 5, 2015
[Down-regulated expression of c-Jun in peripheral blood mononuclear cells of patients with severe secondary pulmonary
Jinwen Su1, Yanhua Liu2, Bingfen Yang2
1Medical College of PLA, Bejing 100853; Institution of Tuberculosis Research, Chinses PLA 309 Hospital, Bejing 100091, China.
Objective:
To compare the expression of c-Jun in severe versus mild secondary pulmonary tuberculosis (TB) and understand the relationship of the c-Jun expression with the inflammation and immune injury of severe secondary TB patients.
Methods:
Differentially expressed genes were screened in patients with severe TB, the ones with mild TB and healthy controls using Affymetrix human gene expression chips. Bioinformatic analysis was performed on the results of the gene chip screening. The relative transcript level of c-Jun was detected by real-time quantitative PCR (qRT-PCR). The protein expression of c-Jun in peripheral blood mononuclear cells was detected by ELISA.
Results:
Patients with severe pulmonary TB exibited a large number of differentially expressed genes compared with healthy controls and patients with mild secondary TB, and these differential expressed genes involved complicated pathways of immue response and inflammation. C-Jun was down-regulated 2.27 times in the patients with severe secondary TB compared with the ones with mild TB, and it is involved in 61 pathways. The qRT-PCR verified that c-Jun was down-regulated significantly in the patients with severe secondary TB compared with the mild ones. ELISA confirmed the trend of down-regulation of c-Jun in the patients with severe secondary TB. The results of qRT-PCR and ELISA were consistent with gene chip analysis.
Conclusion:
C-Jun was down-regulated in the patients with severe secondary TB compared with the patients with mild TB, and it is involved in many pathways of immue response and inflammation. Its down-regulation might be related to the immune injury of severe secondary TB.
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