scholarly journals High Secretion of Interleukin-6 and Increased MINCLE Receptor Expression Upon Exposure to Mycobacterial Cord Factor Analog Trehalose-6, 6-Dibehenate (TDB) in Patients with Takayasu Arteritis

2018 ◽  
Vol 12 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Nikhil Gupta ◽  
Jayakanthan Kabeerdoss ◽  
Hindhumathi Mohan ◽  
Ruchika Goel ◽  
Debashish Danda
Keyword(s):  
Takayasu Arteritis ◽  
Receptor Expression ◽  
Cell Culture Supernatant ◽  
Synthetic Analogue ◽  
Healthy Controls ◽  
Gene Expressions ◽  
Period Gene ◽  
Tnf Α ◽  
Cord Factor ◽  
Type V

Introduction: Suspicion on the association between Takayasu Arteritis (TA) and Tubcerculosis (TB) has been in vogue for years. Prevalence of TB in TA is reported to be higher. We aimed to study innate immune responses in patients with TA on exposure to Trehalose-6,6-dibehenate (TDB), a synthetic analogue of Trehalose-6,6-Dimycolate (TDM, also known as mycobacterial cord factor) in comparison with healthy controls. Materials and Methods: Patients with type V TA, satisfying 1990 ACR criteria, and age and sex matched healthy controls were recruited. PBMCs were cultured with 5µg/ml, 50µg/ml or without any TDB for 48 hours in RPMI medium inside a 5% Co2 incubator. IL-6, TNF-α and IL-17 were measured in cell culture supernatant, which was separated from the cells at the end of the incubation period. Gene expressions of IL-6, IL-8, TNFα, IFN-γ, MINCLE and BCL-10 were quantified in real time PCR using specific primers and SYBR green chemistry. Results: Twenty two TA patients and 21 healthy controls were recruited. Both patients and controls showed response by secreting IL-6 and TNF-α upon stimulation by TDB. Relative induction (TDB stimulated TA sample / unstimulated control) of IL-6 was significantly higher in TA [31.88(0.74-168)] patients as compared to healthy controls [1.931(0.644-8.21); p<0.002], when co-cultured with 50µg/ml TDB. The expression of MINCLE, the TDB receptor was higher in TA samples than healthy controls upon TDB stimulation. Conclusion: Stimulation with mycobacterial synthetic analogue led to higher secretion of IL-6 and higher expression of MINCLE in PBMCs of patients with TA as compared to healthy controls.

scholarly journals Leukocyte toll-like receptor expression in pathergy positive and negative Behçet’s disease patients

Rheumatology ◽  
2020 ◽  
Vol 59 (12) ◽  
pp. 3971-3979
Author(s):  
Tim B van der Houwen ◽  
Willem A Dik ◽  
Marco Goeijenbier ◽  
Manizhah Hayat ◽  
Nicole M A Nagtzaam ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Behçet’S Disease ◽  
Behcet’S Disease ◽  
Behçet's Disease ◽  
Receptor Expression ◽  
Healthy Controls ◽  
Toll Like Receptor ◽  
Behcet's Disease ◽  
Tnf Α ◽  
Classical Monocytes

Abstract Objectives To investigate whether the auto-inflammatory nature and the pathergic reaction in Behçet’s disease (BD) are driven by a disturbed toll-like receptor (TLR) response. Methods We compared both TLR expression by flow-cytometry and TLR response by stimulation assay in 18 BD patients (both pathergy positive and pathergy negative) with 15 healthy controls. Results Expression of TLR1 and 2 was significantly elevated in B-lymphocytes of BD patients compared with healthy controls. TLR1, 2 and 4 were significantly more highly expressed in both CD4+ and CD8+ T-lymphocytes of BD patients. Granulocytes of BD patients displayed significantly higher expression of TLR1, 2, 4 and 6. TLR2, 4 and 5 expression was significantly increased on classical monocytes of BD patients. Intermediate monocytes of BD patients showed an increase in expression of TLR2. Furthermore, TLR2 and 5 were significantly more highly expressed in non-classical monocytes of BD patients. In pathergy positive patients, TLR5 was even more highly expressed compared with pathergy negative patients on B- and T-lymphocytes and granulocytes. Furthermore, TLR2 and 5 showed an elevated TNF-α response to stimulation with their cognate ligands. Conclusion Immune cells of BD patients overexpress TLR1, 2, 4, 5 and 6. Furthermore, after stimulation of TLR2 and 5, BD patients demonstrate a more potent TNF-α response. Although this is a small cohort, in the pathergy positive patients, TLR5 expression is even further augmented, suggesting that a microbial (flagellin) or damage (HMGB1) associated signal may trigger the exaggerated immune response that is characteristic for the pathergy phenomenon in BD. In conclusion, these results point to an exaggerated TLR response in the auto-inflammatory nature of BD.

Production and Expression of Inflammatory Mediators in Leukocytes of Sickle Cell Anaemia Patients and Effects of Hydroxyurea Therapy on This Production

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 2490-2490
Author(s):  
Carolina Lanaro ◽  
Carla Fernanda Franco-Penteado ◽  
Dulcinéia M Albuquerque ◽  
Sara T.O. Saad ◽  
Nicola Conran ◽  
...  
Keyword(s):  
Steady State ◽  
Sickle Cell ◽  
Inflammatory Mediators ◽  
Healthy Controls ◽  
Gene Expressions ◽  
Tnf Α ◽  
Ifn Γ ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Hydroxyurea Therapy

Abstract Leukocytosis is frequently observed in sickle cell disease (SCD) in the absence of bacterial infection. An elevated baseline leukocyte count is associated with an increased risk of early death and leukocytes play a significant role in the initiation of vaso-occlusive events. Inflammation, cell adhesion to vascular endothelium, and subsequent endothelial injury appear to contribute to sickle cell anemia (SCA) vaso-occlusion. Furthermore, blood levels of inflammatory and anti-inflammatory cytokines are reported to be elevated (TNF-α, IL-6, IL-10, GM-CSF), both in steady state and during crisis, but reports have been conflicting and a conclusive role for these molecules in the disease remains to be established. Furthermore, the effect of hydroxyurea therapy (HU) on the release of inflammatory mediators is not understood. The aim of this study was to determine plasma levels and leukocyte gene expressions of inflammatory mediators in healthy controls (n=30), steady-state SCA patients (n=45) and SCA patients on HU therapy (n=24). qRT-PCR analysis was use to examine gene expression and ELISA protein production. TNF-α, IL-8 and PGE2 plasma levels were significantly higher in the plasma of steady-state SCA individuals, when compared to control individuals (2.95 ± 0.4 pg/ml; 16.5 ± 2.5 pg/ml; 5.7 ± 0.6 pg/ml; 128.3 ± 12.2 pg/ml vs 1.43 ± 0.2 pg/ml, 88.5 ± 5.9 pg/ml, P=0.006; P&lt;0.0001; P=0.012, respectively). HU therapy significantly reversed augmented TNF-α (1.6 ± 0.2 pg/ml, P=0.006) and, interestingly, increased plasma anti-inflammatory IL-10 (P&lt;0.05). IL-10, IFN-γ, COX-2 and iNOS gene expressions were unaltered in SCA mononuclear cells (MC), however gene expressions of TNF-α, IL-8 and the protective enzyme, heme oxygenase-1 (HO-1), were significantly higher compared to healthy controls (0.46 ± 0.01; 0.08 ± 0.02; 0.21 ± 0.05 vs 0.18 ± 0.04; 0.02 ± 0.005; 0.035 ± 0.008; respectively, P&lt;0.02). HU therapy was not associated with significantly altered SCA MC inflammatory gene expression, although COX-2 mRNA expression was decreased (0.11 ± 0.05; 0.37 ± 0.12, SCAHU and SCA, respectively; P&lt;0.05). In SCA neutrophils, gene expressions of IL-8, IFN-γ, iNOS and HO-1 were significantly higher compared to those of control subjects (0.32 ± 0.07; 0.69 ± 0.19; 0.19 ± 0.06; 0.33 ± 0.09, P=0.02, P=0.025, P&lt;0.05; P=0.027, respectively). Patients on HU therapy demonstrated lower iNOS and higher IL-10 neutrophil gene expressions compared to SCA not on HU therapy (0.038 ± 0.03; 0.72 ± 0.13, P&lt;0.05; P&lt;0.05, respectively). Taken together, data suggest that alterations in the gene expressions and productions of a number of pro-and anti-inflammatory mediators are present in SCA and knowledge of these pathways may be important for identifying novel drug targets for the disease.

Inflammatory Mediators Are Increased in Leukocytes of IVS-I-6 (T→C) Homozygous β-Thalassemia Intermedia.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4068-4068
Author(s):  
Marcos André C Bezerra ◽  
Carla Fernanda Franco-Penteado ◽  
Carolina Lanaro ◽  
Mariana R. B. Mello ◽  
Sheley Gambero ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Mediators ◽  
Plasma Levels ◽  
Heme Oxygenase 1 ◽  
Mrna Levels ◽  
Healthy Controls ◽  
Thalassemia Intermedia ◽  
Gene Expressions ◽  
Survivin Protein ◽  
Tnf Α

Abstract Abstract 4068 Poster Board III-1003 Thalassemia is characterized by chronic inflammatory state and inflammation may play an important role in the pathogenesis of this diseases. Endothelial adhesion molecules, reactive oxygen species (ROS), C reactive protein and cytokines were increased in thalassemia patients. In addition, adherence of red blood cells, neutrophils and platelets to extracellular matrix protein and neutrophils chemotaxis has been shown to be markedly enhanced in β-thalassemia intermedia (TI) patients. Although alterations in inflammatory biomarkers have been related previously, most studies have been carried out with patients either polytransfused, receiving hydroxyurea (HU) therapy or with β-thalassemia major. An investigation of the role of inflammatory mediators in TI may further contribute to the understanding the pathogenesis of the disease. The aim of this study was to determine plasma levels and leukocyte gene expressions of inflammatory mediators/cytokines in neutrophils and mononuclear cells (MC) of untransfused patients and those not on HU therapy TI IVS-I-6 (T→C) homozygous (n≤20) and healthy controls (n≤20). ELISA was used to determine cytokine production; survivin protein expression was determined by flow cytometry with survivin-specific antibodies and qRT-PCR analysis to examine gene expression of cytokines, the protective enzyme heme oxygenase-1 (HO-1) and BIRC-5 (survivin). TNF-α, IL-6, IL-8 and IL-1β plasma levels were significantly higher in the plasma of TI individuals, when compared to control individuals (3.78 ± 0.4 vs 2.18 ± 0.3; 0.93 ± 0.1 vs 0.46 ± 0.08; 18.97 ± 5.6 vs 6.09 ± 1.1; 1.88 ± 0.7 vs 0.34 ± 0.05, pg/ml, P<0.05, respectively). Survivin protein levels in MC from TI was significantly increased when compared to healthy controls (45.9 ± 1.8 × 39.74 ± 1.74, MFI, P=0.022, respectively). IL-8, IL-10 and HO-1 gene expressions were unaltered in TI neutrophils (0.31 ± 0.13; 0.1 ± 0.08; 0.44 ± 0.2; A.U., respectively) compared to healthy controls neutrophils (0.45 ± 0.13; 0.17 ± 0.04; 0.22 ± 0.07, A.U., respectively), however in TI neutrophils gene expression of TNF-α was significantly higher than those of control subjects (0.76 ± 0.3 vs 0.24 ± 0.05, A.U., P=0.03, respectively). Expressions of genes encoding IL-8, IL-10, HO-1 and BIRC-5 were higher in MC of TI patients, compared with those of healthy controls (0.75 ± 0.3 vs 0.02 ± 0.005; 0.36 ± 0.07 vs 0.19 ± 0.04; 1.69 ± 0.28 vs 0.27 ± 0.09; 1.13 ± 0.12 vs 0.55 ± 0.17, A.U., P=0.02; P=0.04; P=0.0002, P=0.019, respectively). No significant alterations in the TNF-α mRNA levels were found in the MC of TI patients compared with healthy controls (0.21 ± 0.06 vs 0.16 ± 0.03, A.U., respectively). Taken together our data showed a higher production of inflammatory cytokines in MC, which could contribute to the pathophysiology of TI. Anti-inflammatory mechanisms (IL-10 and HO-1) were also up-regulated in these individuals, indicating efforts to counteract these alterations. These results are strong indications of the presence of chronic inflammatory processes and knowledge of these pathways may contribute to the understanding of the pathophysiology of TI. Disclosures: No relevant conflicts of interest to declare.

scholarly journals AB0490 CIRCULATING REGULATORY T CELLS WERE ABSOLUTELY DECREASED IN TAKAYASU’S ARTERITIS PATIENTS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1542.1-1543
Author(s):  
W. Jia ◽  
J. Xie ◽  
X. Wang ◽  
C. Gao ◽  
G. Liu ◽  
...  
Keyword(s):  
Takayasu Arteritis ◽  
Peripheral Blood ◽  
Th17 Cells ◽  
Takayasu’S Arteritis ◽  
Absolute Number ◽  
Treg Cells ◽  
Healthy Controls ◽  
Takayasu's Arteritis ◽  
Tnf Α ◽  
The Absolute

Background:Takayasu arteritis (TA) refers to chronic progressive non-specific inflammation that involves the aorta and its main branches, causing stenosis and occlusion of arteries in different parts, and ischemic manifestations in the corresponding parts. A variety of immune dysfunctions are involved in the occurrence and development of TA(1)Recent studies have shown that Th17/Treg imbalance plays an important role in the pathogenesis of Takayasu’s arteritis, in which T help 17 cells (Th17) cells are up-regulated in TA patients(2). Th17 cells are closely related to Treg cells during differentiation. There are few studies on the expression level of CD4+CD25+FOX3+T lymphocyte (Treg) cells. This study aims to study the clinical significance of Treg cell expression in peripheral blood of patients with Takayasu’s arteritis.Objectives:To analyze the levels of circulating lymphocyte subsets and serum cytokines in patients with takayasu arteritis (TA), and explore the relationship between their changes and TA disease activity.Methods:A total of 46 TA patients and 43 gender-age-matched healthy controls were enrolled. According to the NIH standard, 30 patients were in active disease. Flow cytometry was used to detect the absolute numbers and ratios of Th1, Th2, Th17 and Treg cells in peripheral blood of all subjects. Magnetic bead-based multiplex immunoassay was used to detect cytokines and statistical analysis was performed.Results:Compared with the healthy controls, the absolute number and proportion of peripheral Treg cells of TA patients significantly decreased while those of Th17 cells increased significantly, leading to the increased ratio of Th17 / Treg. Compared with the inactive group, the TA active group had significantly increased IL-6 and TNF-α, and there was no significant difference in the expression of Th17 cells and Treg cells.Conclusion:In peripheral blood of TA patients, Treg cells decreased, while Th17 cells increased as compared with healthay controls, leading to an imbalance between Th17 and Treg cells. The levels of IL-6 and TNF-α were related to disease activity.References:[1]Russo, R.A.G. and M.M. Katsicas, Takayasu Arteritis. Front Pediatr, 2018. 6: p. 265.[2]Misra, D.P., S. Chaurasia, and R. Misra. Increased Circulating Th17 Cells, Serum IL-17A, and IL-23 in Takayasu Arteritis. Autoimmune Dis, 2016. 2016: p. 7841718.Figure 1.Characteristics of the absolute numbers and proportions of Th1cells,Th2cells,Th17 cells and CD4Treg cells in the PB of patients with TA.(A-C)The levels of Th17 cells and the ratio of Th1/Treg,Th2/Treg,Th17/Treg in PB were significantly increased in patients with TA (n=46). The absolute number and the proportion of CD4Treg cells were significantly decreased in TA(n=46). (D-F) The absolute number of Th2 cells and ratio of Th2/Treg in PB were significantly decreased in active patients with TA (n=30).Neither the absolute number nor proporation of Th1, Th17 and Treg cells was altered significantly between active TA patients(n=30) and inactive TA patients(n=16).*P<0.05; **P<0.001. P<0.05 was considered statistically significant.TA,takayasu arteritis;PB peripheral blood;Tregs, regulatory Tcells.Figure 2.Characteristics of serum concentrations of cytokine (including IL-6, IL-10, IL-17 and TNF-α) between active TA patients(n=30) and inactive TA patients(n=16).(A,D)In terms of cytokines, the concentration of IL-6 and TNF-α was significantly up-regulated,(B,C)but no significant changes in IL-10, and IL-17 were found.*P<0.05; **P<0.001. P < 0.05 was considered statistically significant.Disclosure of Interests:None declared

Abstract 339: Ang-(1-7) Counteracts Ang II in Regulating Cerebrovascular Endothelial Cell Function and Gene Expression

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Ji Chen ◽  
Xiang Xiao ◽  
Shuzhen Chen ◽  
Cheng Zhang ◽  
Jinju Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Function ◽  
Tube Formation ◽  
Cell System ◽  
Cell Culture Supernatant ◽  
Complete Medium ◽  
Ang Ii ◽  
Gene Expressions ◽  
Endothelial Cell Function ◽  
Tnf Α

Cerebrovascular endothelial cells (cECs) play an important role in maintaining the health of cerebral vasculatures. In this study, we investigated the role of angiotensin (Ang)-(1-7) in counteracting Ang II-induced effects on cECs. The 3rd-5th passages of brain microvascular endothelial cells (BMECs, Cell system) cultured in CSC complete medium (Cell system) were used for this study. BMECs were treated with Ang II (100 nM), Ang-(1-7) (100 nM) and A-779 (100 nM, Mas receptor antagonist). After treatment for 24 hrs, cell apoptosis was determined by flow cytometery. BMEC tube formation ability was determined using a commercial kit. The levels of tumor necrosis factor- α (TNF-α), monocyte chemoattractant protein 1 (MCP-1) and interleukin (IL-8) in the cell culture supernatant were determined by ELISA. Gene expressions of NFκB, inhibitor of kappa B (IκB) were determined by western blot. To verify the involvement of NFκB pathway, the inhibitor (BAY11-7082, 10 uM) was applied. We found (Figure): 1) Treatment with Ang-(1-7) decreased Ang II-induced apoptosis (22 ± 1.5% vs. 14 ± 1.2%, Ang II vs. Ang II + Ang-(1-7), P<0.01). 2) Ang-(1-7) improved BMEC tube formation ability compromised by Ang II, which was accompanied by up-regulation of IκB expression, the down-regulation of NFκB, and decrease of TNF-α, MCP-1 and IL-8 production of BMECs. 3) These effects of Ang-(1-7) were totally abolished by A-779 and partially blocked by BAY 11-7082. In conclusion, Ang-(1-7)/Mas activation counteracts Ang II-induced BMEC apoptosis and dysfunction, partially via the NFκB dependent inflammation pathway.

CD4+CD25- effector T cells from healthy controls and MS patients do not differ in mRNA expression of IFN-γ, IL-2, and TNF-α

2004 ◽  
Vol 31 (S 1) ◽  
Author(s):  
A Hug ◽  
J Haas ◽  
A Viehöver ◽  
B Fritz ◽  
B Storch-Hagenlocher ◽  
...  
Keyword(s):  
T Cells ◽  
Mrna Expression ◽  
Effector T Cells ◽  
Healthy Controls ◽  
Tnf Α ◽  
Ifn Γ

scholarly journals Do proinflammatory cytokines play a role in clozapine-associated glycometabolism disorders?

2021 ◽  
Author(s):  
Tongtong Zhao ◽  
Kai Zhang ◽  
Yelei Zhang ◽  
Yating Yang ◽  
Xiaoshuai Ning ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Side Effects ◽  
Proinflammatory Cytokines ◽  
Peripheral Blood ◽  
Animal Experiments ◽  
Pancreatic Tissue ◽  
Mouse Serum ◽  
Healthy Controls ◽  
Immunological Mechanisms ◽  
Tnf Α

Abstract Rationale and objective Clozapine (CLZ) is the most effective drug for treatment-resistant schizophrenia but is associated with many side effects, including glycometabolism disorders. Immunological mechanisms may be involved in the development of clozapine side effects. Research relating the immunomodulatory effects of clozapine and its early markers to clinically relevant adverse events is needed to reduce the harmful side effects of clozapine. This study aimed to investigate the role of proinflammatory cytokines in clozapine-associated glycometabolism disorders. Methods We measured the effect of a range of doses of clozapine on glycometabolism-related parameters and proinflammatory cytokines levels in mice peripheral blood. We also examined the differences between these indicators in the peripheral blood of clozapine-treated schizophrenia patients and healthy controls. Furthermore, we detected proinflammatory cytokines expression in mice pancreatic tissue. Results Following clozapine administration, glucagon significantly decreased in mouse serum, and proinflammatory cytokine IL-β levels markedly increased. Clozapine reliably increased proinflammatory cytokines (IL-1β, IL-6, and TNF-α) expression in murine pancreatic tissue. Compared with healthy controls, clozapine-treated patients’ BMI, blood glucose, and proinflammatory cytokines (IL-1β, IL-6, and TNF-α) increased significantly. In clozapine-treated patients, a higher clozapine daily dosage was associated with higher levels of the proinflammatory cytokines IL-1β and IL-6, and a significant positive correlation was observed between blood glucose levels and the proinflammatory cytokines IL-6 and TNF-α. Conclusion Findings from animal experiments and clinical trials have shown clear evidence that clozapine has a regulatory effect on immune-related proinflammatory cytokines and influences glycometabolism indicators.

scholarly journals In Vitro Evaluation of the Anti-Inflammatory Effect of KMUP-1 and in Vivo Analysis of Its Therapeutic Potential in Osteoarthritis

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 615
Author(s):  
Shang-En Huang ◽  
Erna Sulistyowati ◽  
Yu-Ying Chao ◽  
Bin-Nan Wu ◽  
Zen-Kong Dai ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Antioxidant Properties ◽  
Serum Levels ◽  
Gene Expressions ◽  
Tnf Α ◽  
Anti Inflammatory

Osteoarthritis is a degenerative arthropathy that is mainly characterized by dysregulation of inflammatory responses. KMUP-1, a derived chemical synthetic of xanthine, has been shown to have anti-inflammatory and antioxidant properties. Here, we aimed to investigate the in vitro anti-inflammatory and in vivo anti-osteoarthritis effects of KMUP-1. Protein and gene expressions of inflammation markers were determined by ELISA, Western blotting and microarray, respectively. RAW264.7 mouse macrophages were cultured and pretreated with KMUP-1 (1, 5, 10 μM). The productions of TNF-α, IL-6, MMP-2 and MMP- 9 were reduced by KMUP-1 pretreatment in LPS-induced inflammation of RAW264.7 cells. The expressions of iNOS, TNF-α, COX-2, MMP-2 and MMP-9 were also inhibited by KMUP-1 pretreatment. The gene expression levels of TNF and COX families were also downregulated. In addition, KMUP-1 suppressed the activations of ERK, JNK and p38 as well as phosphorylation of IκBα/NF-κB signaling pathways. Furthermore, SIRT1 inhibitor attenuated the inhibitory effect of KMUP-1 in LPS-induced NF-κB activation. In vivo study showed that KMUP-1 reduced mechanical hyperalgesia in monoiodoacetic acid (MIA)-induced rats OA. Additionally, KMUP-1 pretreatment reduced the serum levels of TNF-α and IL-6 in MIA-injected rats. Moreover, macroscopic and histological observation showed that KMUP-1 reduced articular cartilage erosion in rats. Our results demonstrated that KMUP-1 inhibited the inflammatory responses and restored SIRT1 in vitro, alleviated joint-related pain and cartilage destruction in vivo. Taken together, KMUP-1 has the potential to improve MIA-induced articular cartilage degradation by inhibiting the levels and expression of inflammatory mediators suggesting that KMUP-1 might be a potential therapeutic agent for OA.

scholarly journals Phenotypic and Functional Alterations of Immune Effectors in Periodontitis; A Multifactorial and Complex Oral Disease

2021 ◽  
Vol 10 (4) ◽  
pp. 875
Author(s):  
Kawaljit Kaur ◽  
Shahram Vaziri ◽  
Marcela Romero-Reyes ◽  
Avina Paranjpe ◽  
Anahid Jewett
Keyword(s):  
Periodontal Disease ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Oral Disease ◽  
Healthy Controls ◽  
Healthy Individuals ◽  
Tnf Α ◽  
Blood Mononuclear Cells ◽  
Ifn Γ ◽  
And Function

Survival and function of immune subsets in the oral blood, peripheral blood and gingival tissues of patients with periodontal disease and healthy controls were assessed. NK and CD8 + T cells within the oral blood mononuclear cells (OBMCs) expressed significantly higher levels of CD69 in patients with periodontal disease compared to those from healthy controls. Similarly, TNF-α release was higher from oral blood of patients with periodontal disease when compared to healthy controls. Increased activation induced cell death of peripheral blood mononuclear cells (PBMCs) but not OBMCs from patients with periodontal disease was observed when compared to those from healthy individuals. Unlike those from healthy individuals, OBMC-derived supernatants from periodontitis patients exhibited decreased ability to induce secretion of IFN-γ by allogeneic healthy PBMCs treated with IL-2, while they triggered significant levels of TNF-α, IL-1β and IL-6 by untreated PBMCs. Interaction of PBMCs, or NK cells with intact or NFκB knock down oral epithelial cells in the presence of a periodontal pathogen, F. nucleatum, significantly induced a number of pro-inflammatory cytokines including IFN-γ. These studies indicated that the relative numbers of immune subsets obtained from peripheral blood may not represent the composition of the immune cells in the oral environment, and that orally-derived immune effectors may differ in survival and function from those of peripheral blood.

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