Abstract:
:Rheumatoid arthritis (RA) is a high morbidity and disability disease with numerous inflammatory cells infiltrating in interstitial of articular cartilages and bones. As the most abundant inflammatory cells, neutrophil has been reported that their apoptosis changed gradually in the circumstance of RA. Apoptosis, one modality of programmed cell death (PCD), is closely associated with autophagy, which indicates neutrophil autophagy may also alter in RA. Flow cytometry, western blotting, immunohistochemistry, immunofluorescence, transmission electron microscope and multiplex antibody microarray were used to comparative investigate the status of neutrophil autophagy in patients with RA and in vitro. The results showed that the expression of autophagy related LC3 protein was up-regulated with lower lysosomal pH in neutrophils from synovial fluid of RA and changed under stimulation of CQ and small RNA interferences (siRNAs) Atg5 transfection, which proved in acute promyelocytic leukemia HL-60 cell lines, predominantly a neutrophilic promyelocyte, treated by plasma and synovial fluid from RA. We further found out the concentration of IL-6, IL-8, IL-10 and MCP-1 was higher in their synovial fluid which may mediate neutrophil autophagy in RA via cytokine-cytokine receptor interaction and IL-17 signaling pathway. Our results indicate that neutrophil autophagy may be a novel perspective to understand the pathology which may provide a new maker to diagnose RA and IL-8, IL-10, MCP-1 specific antagonists and neutrophil autophagy target inhibitors may improve the therapeutic effect of RA someday.
journal_name
Int Immunopharmacoljournal_title
International immunopharmacologyauthors
An Q,Yan W,Zhao Y,Yu Kdoi
10.1016/j.intimp.2018.09.011subject
Has Abstractpub_date
2018-12-01 00:00:00pages
119-128eissn
1567-5769issn
1878-1705pii
S1567-5769(18)30602-7journal_volume
65pub_type
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journal_title:International immunopharmacology
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journal_title:International immunopharmacology
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journal_title:International immunopharmacology
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journal_title:International immunopharmacology
pub_type: 杂志文章,meta分析,评审
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journal_title:International immunopharmacology
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pub_type: 杂志文章,评审
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journal_title:International immunopharmacology
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journal_title:International immunopharmacology
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pub_type: 杂志文章
doi:10.1016/j.intimp.2018.01.028
更新日期:2018-03-01 00:00:00
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journal_title:International immunopharmacology
pub_type: 杂志文章
doi:10.1016/s1567-5769(02)00018-8
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journal_title:International immunopharmacology
pub_type: 杂志文章
doi:10.1016/j.intimp.2012.03.012
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journal_title:International immunopharmacology
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doi:10.1016/j.intimp.2008.03.011
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journal_title:International immunopharmacology
pub_type: 杂志文章
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更新日期:2020-04-01 00:00:00
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journal_title:International immunopharmacology
pub_type: 杂志文章
doi:10.1016/S1567-5769(03)00202-9
更新日期:2003-11-01 00:00:00
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journal_title:International immunopharmacology
pub_type: 杂志文章
doi:10.1016/j.intimp.2014.01.009
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journal_title:International immunopharmacology
pub_type: 杂志文章
doi:10.1016/j.intimp.2020.106633
更新日期:2020-08-01 00:00:00
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journal_title:International immunopharmacology
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journal_title:International immunopharmacology
pub_type: 杂志文章
doi:10.1016/j.intimp.2014.04.026
更新日期:2014-08-01 00:00:00
abstract:BACKGROUND:Many studies have shown that ghrelin can down-regulate inflammatory cytokine expression via the inhibition of NF-κB activity and therefore, its administration to septic patients is considered beneficial. However, our knowledge of ghrelin's effects on the upstream activators of the NF-κB pathway, such as NOD2...
journal_title:International immunopharmacology
pub_type: 杂志文章
doi:10.1016/j.intimp.2012.04.006
更新日期:2012-08-01 00:00:00
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journal_title:International immunopharmacology
pub_type: 杂志文章
doi:10.1016/j.intimp.2010.11.034
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