Abstract:
BACKGROUND:Rheumatoid arthritis (RA) is a chronic autoimmune disease, which causes synovial damage. Persistence of lymphocyte infiltrates in the rheumatoid synovium has been attributed to abnormal apoptosis. While not comprehensively investigated, perturbations in peripheral blood lymphocyte (PBL) apoptosis may also be involved in perpetuation of autoimmune processes in RA. METHODS:We investigated total, CD4+ and CD19+ PBL apoptosis in our study cohort by monitoring the translocation of phosphatidylserine using the Annexin-V assay. To examine the role of death receptor mediated apoptosis as well as activation-induced-cell-death (AICD), PBLs were labeled with CD95/Fas and CD69 markers and enumerated by flow cytometry. Proteolytic activity of initiator and executioner caspases was determined by luminometry. DNA fragmentation assays were used to examine whether apoptotic signals were transduced to the nucleus. Quantitative PCR arrays were used to investigate apoptotic pathways associated with RA-PBLs. Since heat-shock-protein-70 (HSP70) is an inducible protein which modulates apoptotic signals, we determined HSP70 levels by intra-cellular flow cytometry and western blots. RESULTS:The RA-PBLs showed signs of elevated apoptosis whilst in circulation. These include increases in the loss of plasma membrane asymmetry, indicated by increased externalization of phosphatidylserine (especially in B-lymphocytes). RA-PBLs showed a bias to CD95/Fas mediated apoptotic pathways, but low levels of the CD69 marker suggested that this was not associated with immune activation. Although downstream markers of apoptosis such as caspase-3/7 activity, were increased, no DNA fragmentation was observed in RA-PBLs. Interestingly, elevated levels of apoptosis did not correlate with absolute lymphocyte counts in RA patients. Levels of HSP70 were highly elevated in RA-PBLs compared to controls. CONCLUSION:The results suggest that while apoptosis may be initiated in RA-PBLs, they may lack commitment to fully executing the apoptotic program. This may be related to inhibition on apoptotic transduction by HSP70. This study provides evidence that abnormalities in RA-PBLs apoptosis may occur whilst still in circulation and may contribute to pathogenesis of the disease.
journal_name
J Inflamm (Lond)journal_title
Journal of inflammation (London, England)authors
Moodley D,Mody GM,Chuturgoon AAdoi
10.1186/1476-9255-8-30subject
Has Abstractpub_date
2011-11-03 00:00:00pages
30issue
1issn
1476-9255pii
1476-9255-8-30journal_volume
8pub_type
杂志文章abstract:: The intestinal immune system and the epithelium are the first line of defense in the gut. Constantly exposed to microorganisms from the environment, the gut has complex defense mechanisms to prevent infections, as well as regulatory pathways to tolerate commensal bacteria and food antigens. Intestinal pathogens have ...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-8-11
更新日期:2011-05-03 00:00:00
abstract:BACKGROUND:Chronic spontaneous urticaria (CSU) is an immune-inflammatory disease, characterized by acute phase response (APR) and immune activation. There has been increasing evidence showing that vitamin D deficiency/insufficiency is associated with increased incidence and/or severity of immune-inflammatory disorders....
journal_title:Journal of inflammation (London, England)
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abstract:BACKGROUND:CCR2 plays a key role in regulating monocyte trafficking to sites of inflammation and therefore has been the focus of much interest as a target for inflammatory disease. METHODS:Here we examined the effects of CCR2 blockade with a potent small molecule antagonist to determine the pharmacodynamic consequence...
journal_title:Journal of inflammation (London, England)
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doi:10.1186/1476-9255-6-32
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abstract:BACKGROUND:Salivary histatins are bioactive peptides related to the innate immune system associated with antimicrobial activities. However, very little is known about the physiological and biological functions of histatins against host cells or their role in oral cell inflammation. Histatin 3 binds to heat shock cognat...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-11-4
更新日期:2014-02-04 00:00:00
abstract:BACKGROUND:Heat shock protein 90 (Hsp90), a chaperone that regulates activity of many client proteins responsible for cellular growth, differentiation, and apoptosis, has been proposed as an important clinical and preclinical therapeutic target in a number of malignancies and autoimmune diseases, respectively. In this ...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-11-10
更新日期:2014-04-02 00:00:00
abstract:: Tumor necrosis factor alpha (TNF-alpha)is a host inflammatory factor. Bacteria increase TNF-alpha expression in a variety of human diseases including infectious diseases, inflammatory bowel diseases, and cancer. It is unknown, however, how TNF-alpha directly modulates bacterial protein expression during intestinal in...
journal_title:Journal of inflammation (London, England)
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abstract::Adult bone marrow derived mesenchymal stem cells offer the potential to open a new frontier in medicine. Regenerative medicine aims to replace effete cells in a broad range of conditions associated with damaged cartilage, bone, muscle, tendon and ligament. However the normal process of immune rejection of mismatched a...
journal_title:Journal of inflammation (London, England)
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abstract:BACKGROUND:Monocytes and neutrophils are examples of phagocytic leukocytes, with neutrophils being considered as the 'chief' phagocytic leukocyte. Both monocytes and neutrophils have been implicated to play a key role in the development of ischaemia-reperfusion injury, where they are intrinsically involved in leukocyte...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-4-12
更新日期:2007-05-30 00:00:00
abstract::Cathelicidins are mammalian proteins containing a C-terminal cationic antimicrobial domain. Porcine PR-39 cathelicidin affects leukocyte biology. Mechanisms of action may involve alteration of heparan sulfate proteoglycan-dependent functions in inflammatory cells. It was tested whether PR-39 affects human neutrophil m...
journal_title:Journal of inflammation (London, England)
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abstract:BACKGROUND:Activation of NADPH oxidase is required for neutrophil extracellular trap (NET) formation. Protein kinase C (PKC) is an upstream mediator of NADPH oxidase activation and thus likely to have a role in NET formation. METHODS:Pharmacological inhibitors were used to block PKC activity in neutrophils harvested f...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-10-12
更新日期:2013-03-21 00:00:00
abstract:BACKGROUND:Urinary bladder and renal dysfunction are secondary events associated with spinal cord injury (SCI) in humans. These secondary events not only compromise quality of life but also delay overall recovery from SCI pathophysiology. Furthermore, in experimental models the effects of SCI therapy on bladder and ren...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-3-15
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abstract::Athrosclerosis is conceived as a chronic inflammatory status affecting cells from vascular walls. Different mechanisms and pathological features are evident at the onset of atherosclerotic changes via the engaging different cells from the vascular wall and circulatory cells. Attempts are currently focused on the detec...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章,评审
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abstract:BACKGROUND:Toll-like receptors (TLRs) are recognized as important contributors to the initiation and modulation of the inflammatory response in the eye. This study investigated the precise expression patterns and functionality of TLRs in human corneal epithelial cells (HCE) and in conjunctival fibroblasts (HCF). METHO...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-11-3
更新日期:2014-02-04 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/s12950-019-0233-z
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章,评审
doi:10.1186/s12950-017-0174-3
更新日期:2017-11-21 00:00:00
abstract:BACKGROUND:Milk-derived bioactive peptides retain many biological properties and have therapeutic effects in cardiovascular disorders such as atherosclerosis. Under inflammatory conditions the expression of endothelial cells adhesion molecules is induced, increasing monocyte adhesion to human vessel wall, a critical st...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/s12950-014-0044-1
更新日期:2015-01-20 00:00:00
abstract:BACKGROUND:Intracranial infection, one of the complications of traumatic brain injury, is usually associated with inflammation. Several microRNAs (miRNAs), including miR-155, have been reported to be critical modulators in peripheral and central nervous system inflammation. In this study, we investigated the role of mi...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/s12950-017-0162-7
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-10-36
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abstract:Background:Impairment of the blood-brain barrier (BBB) in severe acute pancreatitis (SAP) could result in life-threatening pancreatic encephalopathy. Interleukin-10 (IL-10) is a classical cytokine that is well-known for its strong immunoregulatory and anti-inflammatory abilities. However, whether and how IL-10 protects...
journal_title:Journal of inflammation (London, England)
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-3-1
更新日期:2006-01-27 00:00:00
abstract:BACKGROUND:Nuclear factor kappa B (NF-kappaB) has been shown to play an important role in regulating the expression of many genes involved in cell survival, immunity and in the inflammatory processes. NF-kappaB activation upregulates inducible nitric oxide synthase leading to enhanced nitric oxide production during an ...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-4-23
更新日期:2007-11-24 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-5-7
更新日期:2008-05-29 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-10-3
更新日期:2013-01-31 00:00:00
abstract:BACKGROUND:Airway inflammation and asthma have been linked to oxidative stress and the melastatin-related transient receptor potential cation channel, member 2 (TRPM2), which can be activated by reactive oxygen species (ROS), has emerged as a potential therapeutic target for inflammatory diseases. OBJECTIVE:Using TRPM...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-10-19
更新日期:2013-05-01 00:00:00
abstract:BACKGROUND:Hemorrhagic shock/resuscitation is associated with aberrant neutrophil activation and organ failure. This experimental porcine study was done to evaluate the effects of Fas-directed extracorporeal immune therapy with a leukocyte inhibition module (LIM) on hemodynamics, neutrophil tissue infiltration, and tis...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-7-18
更新日期:2010-04-20 00:00:00
abstract:BACKGROUND:Toll-like receptor (TLR) activation is hypothesized to contribute to inflammatory eye disease including uveitis, yet the distribution pattern of TLRs in human uveal tissues remains poorly described. The purpose of this study was to investigate the expression profile of TLRs in human iris pigment epithelial c...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-11-20
更新日期:2014-07-16 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/s12950-015-0093-0
更新日期:2015-07-28 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-2-9
更新日期:2005-08-09 00:00:00