Increased complement C1q level marks active disease in human tuberculosis.

<h4>Background</h4>Complement functions as an important host defense system and complement C5 and C7 have been implicated in immunopathology of tuberculosis. However, little is known about the role of other complement components in tuberculosis.<h4>Methods</h4>Complement gene...

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Main Authors: Yi Cai, Qianting Yang, Yueqiang Tang, Mingxia Zhang, Haiying Liu, Guoliang Zhang, Qunyi Deng, Jian Huang, Zhiliang Gao, Boping Zhou, Carl G Feng, Xinchun Chen
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24647646/pdf/?tool=EBI
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spelling doaj-21e19555e07243b7bb7473739f11940f2021-03-04T09:40:13ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0193e9234010.1371/journal.pone.0092340Increased complement C1q level marks active disease in human tuberculosis.Yi CaiQianting YangYueqiang TangMingxia ZhangHaiying LiuGuoliang ZhangQunyi DengJian HuangZhiliang GaoBoping ZhouCarl G FengXinchun Chen<h4>Background</h4>Complement functions as an important host defense system and complement C5 and C7 have been implicated in immunopathology of tuberculosis. However, little is known about the role of other complement components in tuberculosis.<h4>Methods</h4>Complement gene expression in peripheral blood mononuclear cells of tuberculosis patients and controls were determined using whole genome transcriptional microarray assays. The mRNA and protein levels of three C1q components, C1qA, C1qB, and C1qC, were further validated by qRT-PCR and enzyme-linked immunosorbent assay, respectively. The percentages of C1q expression in CD14 positive cells were determined by flow cytometry. Finally, C1qC protein level was quantified in the pleural fluid of tuberculosis and non-tuberculosis pleurisy.<h4>Results</h4>C1q expression increases significantly in the peripheral blood of patients with active tuberculosis compared to healthy controls and individuals with latent TB infection. The percentage of C1q-expressing CD14 positive cells is significantly increased in active TB patients. C1q expression in the peripheral blood correlates with sputum smear positivity in tuberculosis patients and is reduced after anti-tuberculosis chemotherapy. Notably, receiver operating characteristic analysis showed that C1qC mRNA levels in peripheral blood efficiently discriminate active from latent tuberculosis infection and healthy controls. Additionally, C1qC protein level in pleural effusion shows improved power in discriminating tuberculosis from non-tuberculosis pleurisy when compared to other inflammatory markers, such as IL-6 and TNF-α.<h4>Conclusions</h4>C1q expression correlates with active disease in human tuberculosis. C1q could be a potential diagnostic marker to discriminate active tuberculosis from latent tuberculosis infection as well as tuberculosis pleurisy from non-tuberculosis pleurisy.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24647646/pdf/?tool=EBI
collection DOAJ
language English
format Article
sources DOAJ
author Yi Cai
Qianting Yang
Yueqiang Tang
Mingxia Zhang
Haiying Liu
Guoliang Zhang
Qunyi Deng
Jian Huang
Zhiliang Gao
Boping Zhou
Carl G Feng
Xinchun Chen
spellingShingle Yi Cai
Qianting Yang
Yueqiang Tang
Mingxia Zhang
Haiying Liu
Guoliang Zhang
Qunyi Deng
Jian Huang
Zhiliang Gao
Boping Zhou
Carl G Feng
Xinchun Chen
Increased complement C1q level marks active disease in human tuberculosis.
PLoS ONE
author_facet Yi Cai
Qianting Yang
Yueqiang Tang
Mingxia Zhang
Haiying Liu
Guoliang Zhang
Qunyi Deng
Jian Huang
Zhiliang Gao
Boping Zhou
Carl G Feng
Xinchun Chen
author_sort Yi Cai
title Increased complement C1q level marks active disease in human tuberculosis.
title_short Increased complement C1q level marks active disease in human tuberculosis.
title_full Increased complement C1q level marks active disease in human tuberculosis.
title_fullStr Increased complement C1q level marks active disease in human tuberculosis.
title_full_unstemmed Increased complement C1q level marks active disease in human tuberculosis.
title_sort increased complement c1q level marks active disease in human tuberculosis.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2014-01-01
description <h4>Background</h4>Complement functions as an important host defense system and complement C5 and C7 have been implicated in immunopathology of tuberculosis. However, little is known about the role of other complement components in tuberculosis.<h4>Methods</h4>Complement gene expression in peripheral blood mononuclear cells of tuberculosis patients and controls were determined using whole genome transcriptional microarray assays. The mRNA and protein levels of three C1q components, C1qA, C1qB, and C1qC, were further validated by qRT-PCR and enzyme-linked immunosorbent assay, respectively. The percentages of C1q expression in CD14 positive cells were determined by flow cytometry. Finally, C1qC protein level was quantified in the pleural fluid of tuberculosis and non-tuberculosis pleurisy.<h4>Results</h4>C1q expression increases significantly in the peripheral blood of patients with active tuberculosis compared to healthy controls and individuals with latent TB infection. The percentage of C1q-expressing CD14 positive cells is significantly increased in active TB patients. C1q expression in the peripheral blood correlates with sputum smear positivity in tuberculosis patients and is reduced after anti-tuberculosis chemotherapy. Notably, receiver operating characteristic analysis showed that C1qC mRNA levels in peripheral blood efficiently discriminate active from latent tuberculosis infection and healthy controls. Additionally, C1qC protein level in pleural effusion shows improved power in discriminating tuberculosis from non-tuberculosis pleurisy when compared to other inflammatory markers, such as IL-6 and TNF-α.<h4>Conclusions</h4>C1q expression correlates with active disease in human tuberculosis. C1q could be a potential diagnostic marker to discriminate active tuberculosis from latent tuberculosis infection as well as tuberculosis pleurisy from non-tuberculosis pleurisy.
url https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24647646/pdf/?tool=EBI
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