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Cytokine Pattern (cytokine + pattern)

Distribution by Scientific Domains

Medical Sciences	84%
Life Sciences	15%

Selected Abstracts

Cytokine pattern determines the progression of experimental periodontal disease induced by Actinobacillus actinomycetemcomitans through the modulation of MMPs, RANKL, and their physiological inhibitors

MOLECULAR ORAL MICROBIOLOGY, Issue 1 2006
G. P. Garlet
Objective:, Inflammatory and immune reactions raised in response to periodontopathogens are thought to trigger periodontal tissue destruction. We therefore investigated the expression of matrix metalloproteinases (MMPs) and the osteoclastogenic factor RANKL (receptor activator of nuclear factor-,B ligand), their respective inhibitors TIMPs (tissue inhibitors of metalloproteinases) and OPG (osteoprotegerin) and their possible correlation with the expression of inflammatory and regulatory cytokines in the course of experimental periodontal disease in mice. Methods:, We characterized the time course of leukocyte migration and alveolar bone loss in C57BL/6 mice infected with Actinobacillus actinomycetemcomitans. Quantitative polymerase chain reaction (RealTime PCR) and ELISA were performed to determine the expression of MMPs, TIMPs, RANKL, OPG and cathepsin K, interleukin-1,, tumor necrosis factor-,, interferon-,, interleukin-12, interleukin-4 and interleukin-10 in periodontal tissue samples harvested throughout the course of experimental disease. Results:, Oral inoculation of A. actinomycetemcomitans results in an intense and widespread migration of leukocytes to the gingival tissues, besides marked alveolar bone resorption. Our data also demonstrate two distinct patterns of MMP/TIMP and RANKL/OPG expression in the course of experimental periodontal disease. The expression of MMPs (MMP-1, 2 and 9) and RANKL was correlated with the expression of interleukin-1,, tumor necrosis factor-, and interferon-,, in a time period characterized by the intense increase of inflammatory reaction and alveolar bone loss. On the other hand, interleukin-4 and interleukin-10 were associated with higher expression of TIMPs (TIMP 1, 2 and 3) and OPG, with a lower expression of MMPs and RANKL, and with reduced rates of increase of cellular infiltration in periodontal tissues and alveolar bone loss. Conclusions:, It is possible that the pattern of cytokines produced in periodontal tissues determines the progression and the severity of experimental periodontal disease, controlling the breakdown of soft and bone tissues through the balance between MMPs/TIMP and RANKL/OPG expression in gingival tissues. [source]

Human resting CD16,, CD16+ and IL-2-, IL-12-, IL-15- or IFN-,-activated natural killer cells differentially respond to sphingosylphosphorylcholine, lysophosphatidylcholine and platelet-activating factor

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 9 2005
Yixin Jin
Abstract The phosphorylcholine-containing lipid lysophosphatidylcholine (LPC) is abundant in the bloodstream, whereas sphingosylphosphorylcholine (SPC) and platelet-activating factor (PAF) highly accumulate at inflamed sites. Utilizing RT-PCR, flow cytometry and immunoblot analyses, we show for the first time that ovarian cancer G,protein-coupled receptor,1, the receptor for SPC, is expressed in IL-2-, IL-12- and IL-15-activated but not in resting CD16,, resting CD16+ or IFN-,-activated NK,cells. Similarly, G2 accumulation and PAF receptor are variably expressed in these subsets of NK,cells. SPC, LPC and PAF differentially induce the chemotaxis of resting and activated NK,cells. In the chemotaxis assay, it is observed that resting CD16,CD56bright and CD16+CD56dim cells predominantly respond to LPC, whereas activated NK,cells, regardless of the sort of stimulus, robustly respond to PAF. SPC is also a potent chemoattractant for IL-2-, IL-12- and IL-15- but not for IFN-,-activated NK,cells. Further analysis shows that, depending on the cytokine pattern of NK,cell activation, phosphorylcholine-containing lipids differentially affect IFN-, secretion by these cells. Our results provide one possible explanation for the tissue compartmentation of NK,cells and their ability to secrete IFN-,. Furthermore, these results may provide novel information regarding NK,cell regulation during inflammation. [source]

Treatment with testosterone or estradiol in melatonin treated females and males MRL/MpJ-Faslpr mice induces negative effects in developing systemic lupus erythematosus

JOURNAL OF PINEAL RESEARCH, Issue 2 2008
Antonio J. Jimenez-Caliani
Abstract:, MRL/MpJ-Faslpr mice is widely accepted as a valuable model of systemic lupus erythematosus. As described in a previous work, the incidence of lupus in this strain is determined by sex hormones, i.e., estrogens and androgens. Moreover, we reported that the immunomodulatory action of melatonin in these mice was gender-dependent probably through modulation and inhibition of sex hormones. Herein, we performed an experiment using hormone therapy, by treating female MRL-lpr mice with testosterone and males with estradiol and with melatonin. A decrease in total serum immunoglobulin (Ig)G and IgM immunoglobulin titers, anti-double-stranded DNA, and anti-CII autoantibodies in female mice treated with both melatonin and testosterone was revealed, along with an increase in pro-inflammatory cytokines [interleukin (IL)-2, IL-6, interferon-,, tumor necrosis factor-,, and IL-1,), nitrite/nitrate and a decrease in anti-inflammatory cytokines (IL-10). Melatonin and estradiol treatment exhibited a similar effect in male mice. Autoantibody titer elevation and pro-inflammatory versus anti-inflammatory cytokine prevalence degraded all immunological parameters. Similar results were obtained when spleen and lymph node lymphocytes were cultured. Again, melatonin and testosterone treatment stimulated pro-inflammatory and reduced anti-inflammatory cytokines produced by lymphocytes in females. The effect was similar in males treated with melatonin and estradiol. In summary, we observed that although melatonin alone prevents lupus development in females, adding testosterone, increased pro-inflammatory cytokine pattern. In contrary, estradiol-treated males did not show any decrease in pro-inflammatory cytokines but showed an increase in regard to melatonin controls. These findings confirm that melatonin action in MRL/MpJ-Faslpr mice could be gender-dependent through modulation of sex hormones. [source]

Vaccination against hepatitis B in liver transplant recipients: Pilot analysis of cellular immune response shows evidence of HBsAg-specific regulatory T cells

LIVER TRANSPLANTATION, Issue 3 2007
Tanja Bauer
After liver transplantation for hepatitis-B-related diseases, patients currently receive lifelong treatment with hepatitis B immunoglobulin to prevent endogenous reinfection with hepatitis B virus (HBV). Active immunization with hepatitis B vaccine would be a preferable alternative; however, most attempts to immunize these patients with standard vaccine have failed. A recent study with a new adjuvanted hepatitis B vaccine was exceptionally successful, leading to a high-titered long-lasting antibody response in 80% of all vaccinees. To identify the immunological mechanisms behind these unexpected results, the successfully vaccinated participants were tested for hepatitis B surface antigen (HBsAg)-specific T and B cells, and their cellular responses to revaccination with conventional vaccine were studied. HBsAg-specific CD4+ T lymphocytes could be detected in 13 of 16 patients after immunization with the new vaccine. Unexpectedly, these T cells produced almost exclusively interleukin (IL)-10 and had a CD4+/CD25+ phenotype. They were functionally active, suppressing cytokine secretion in HBsAg-specific (Th1) cells, thus representing antigen-specific regulatory T cells (TReg). Following a booster dose with conventional vaccine 22-31 months after completion of the initial vaccination series, the T-cell pattern in the revaccinated individuals changed substantially: 7 days after revaccination 9 of 11 individuals showed a switch to a Th1-type immune response with HBsAg-specific T cells secreting IL-2, interferon gamma and tumor necrosis factor alpha as observed in healthy controls. Four weeks after the booster, 4 patients still showed a Th1-type cytokine pattern, whereas in 5 patients only IL-10-secreting cells were detectable. After 1 year, in 3 of 4 revaccinated individuals only IL-10-secreting cells could be found, whereas the specific T cells of the fourth patient still showed a Th1-type of response. HBsAg-specific TReg cells could be demonstrated in HBV-positive liver transplant recipients successfully immunized with a new adjuvanted vaccine. Revaccination led to immediate disappearance of the these cells and the appearance of HBsAg-specific T cells with a Th1-type cytokine profile, which in most cases were replaced by the IL-10-secreting regulatory cells during the following months. The specific induction of TReg cells could contribute to the poor response of liver transplant recipients to conventional vaccine. In conclusion,, for successful vaccination of these patients, a vaccine with a strong inhibitory effect on TReg cells would be desirable. Liver Transpl 13:434,442, 2007. © 2007 AASLD. [source]

Mycobacterial heat shock protein-induced blood T lymphocytes subsets and cytokine pattern: Comparison of sarcoidosis with tuberculosis and healthy controls

RESPIROLOGY, Issue 3 2007
Anna DUBANIEWICZ
Background and objective: Sarcoidosis (SA) is a disorder of unknown aetiology. Mycobacterium tuberculosis heat shock proteins (Mtb-hsp) have been considered as causative agents of SA. The role of Mtb-hsp in the immune response in SA has not been investigated. Methods: Mtb-hsp-stimulated T-cell subsets and Th1/Th2 cytokine patterns in the supernatant from peripheral blood mononuclear cell cultures from 22 SA patients, 20 tuberculosis (TB) patients and 20 healthy volunteers were compared using flow cytometry. Results: In unstimulated cultures, a significantly higher percentage of CD8+,,+T-cells were present in SA versus controls. Similarly there was a significantly increased IL-6 and decreased IL-4 level in SA and significantly lower INF-,, IL-2, IL-4, IL-10 production in TB versus controls. After Mtb-hsp stimulation, there was a significantly increased TNF-,, IL-6, IL-10 and decreased INF-,, IL-2, IL-4 production in SA and significantly increased TNF-,, IL-6 concentrations in TB versus controls. CD8+,,+IL-4+T-cells were detected significantly less often in Mtb-hsp-induced cultures in SA versus controls. Comparing SA versus TB, CD4+,,+TCR-cells were significantly increased in Mtb-hsp-induced cultures in TB versus controls and SA. Before stimulation, significantly increased IL-6, IL-10 and decreased IL-4 level in SA versus TB was revealed, whereas Mtb-hsp stimulation caused significantly increased IL-10 and decreased IL-4 concentrations in SA. Conclusions: After Mtb-hsp stimulation, increased levels of pro-inflammatory cytokines, TNF-, and IL-6 were found in sera from SA and TB patients in comparison with healthy controls; SA patients demonstrated the lowest levels of IL-4 and the highest levels of IL-10. [source]

Dendritic cells lentivirally engineered to overexpress interleukin-10 inhibit contact hypersensitivity responses, despite their partial activation induced by transduction-associated physical stress

THE JOURNAL OF GENE MEDICINE, Issue 3 2010
Verena Besche
Abstract Background Dendritic cells (DCs) constitute an attractive target for immunotherapeutic approaches. Because DCs are largely refractory to transfection with plasmid DNA, several viral transduction protocols were established. The potential side-effects of lentiviral transduction on the phenotype and activation state of DCs left unstimulated after transduction have not been assessed. There is a need to analyse these parameters as a result of the requirement of using DCs with a low activation state for therapeutic strategies intended to induce tolerance. Methods Lentivirally-transduced bone marrow (BM)-derived DCs (LV-DCs) in comparison with mock-transduced (Mock-DCs) and untreated DCs were analysed with regard to the induction of maturation processes on the RNA, protein and functional level. BM-DCs engineered to overexpress interleukin (IL)-10 were analysed for therapeutic potential in a mouse model of allergic contact dermatitis. Results Compared with untreated DCs, Mock-DCs and LV-DCs displayed an altered gene expression signature. Mock-DCs induced a stronger T cell proliferative response than untreated DCs. LV-DCs did not further augment the T cell proliferative response, but induced a slightly different T cell cytokine pattern compared to Mock-DCs. Accordingly, the gene promoter of the DC maturation marker fascin mediated efficient expression of the model transgene IL-10 in unstimulated-transduced BM-DCs. Nevertheless, IL-10 overexpressing BM-DCs exerted tolerogenic activity and efficiently inhibited the contact hypersensitivity response in previously hapten-sensitized mice. Conclusions Lentiviral transduction of BM-DCs results in their partial activation. Nevertheless, the transduction of these DCs with a vector encoding the immunomodulatory cytokine IL-10 rendered them tolerogenic. Thus, lentivirally-transduced DCs expressing immunomodulatory molecules represent a promising tool for induction of tolerance. Copyright © 2010 John Wiley & Sons, Ltd. [source]

The PTPN22 C1858T polymorphism is associated with skewing of cytokine profiles toward high interferon-, activity and low tumor necrosis factor , levels in patients with lupus

ARTHRITIS & RHEUMATISM, Issue 9 2008
Silvia N. Kariuki
Objective The C1858T polymorphism in PTPN22 has been associated with the risk of systemic lupus erythematosus (SLE) as well as multiple other autoimmune diseases. We have previously shown that high serum interferon-, (IFN,) activity is a heritable risk factor for SLE. The aim of this study was to determine whether the PTPN22 risk variant may shift serum cytokine profiles to higher IFN, activity, resulting in risk of disease. Methods IFN, was measured in 143 patients with SLE, using a functional reporter cell assay, and tumor necrosis factor , (TNF,) was measured by enzyme-linked immunosorbent assay. The rs2476601 single-nucleotide polymorphism in PTPN22 (C1858T) was genotyped in the same patients. Patients were grouped, using a clustering algorithm, into 4 cytokine groups (IFN, predominant, IFN, and TNF, correlated, TNF, predominant, and both IFN, and TNF, low). Results SLE patients carrying the risk allele of PTPN22 had higher serum IFN, activity than patients lacking the risk allele (P = 0.027). TNF, levels were lower in carriers of the risk allele (P = 0.030), and the risk allele was more common in patients in the IFN,-predominant and IFN, and TNF,-correlated groups as compared with patients in the TNF,-predominant and both IFN, and TNF,-low groups (P = 0.001). Twenty-five percent of male patients carried the risk allele, compared with 10% of female patients (P = 0.024); however, cytokine skewing was similar in both sexes. Conclusion The autoimmune disease risk allele of PTPN22 is associated with skewing of serum cytokine profiles toward higher IFN, activity and lower TNF, levels in vivo in patients with SLE. This serum cytokine pattern may be relevant in other autoimmune diseases associated with the PTPN22 risk allele. [source]

Interferon- ,1b treatment modulates cytokines in patients with primary progressive multiple sclerosis

ACTA NEUROLOGICA SCANDINAVICA, Issue 6 2006
A. Dressel
Objectives,,, It is unknown whether the immunological effects of , -interferon (IFN- ,) differ in primary progressive multiple sclerosis (PPMS) when compared with relapsing,remitting multiple sclerosis (RRMS). Therefore, we investigated the effects of IFN- ,1b treatment in PPMS on proliferation and cytokine pattern of peripheral blood mononuclear cells (PBMC) and interleukin-10 (IL-10) serum level. Methods,,, Eighteen patients were treated with IFN- ,1b for 12 months in an open-label trial. Serum and PBMC were collected longitudinally. Results,,, Interleukin-10 serum levels increased (P = 0.02) during treatment. Tumor necrosis factor- , was increased in anti CD3 (OKT3) antibody stimulated PBMC during treatment (P = 0.04), whereas secretion of IL-10 was decreased in OKT3 (P = 0.04), but increased in concavalin A stimulated PBMC (P = 0.02). Conclusions,,, Interleukin-10 serum levels rose in IFN- ,1b-treated patients as has been observed in RRMS. The changes in cytokine patterns secreted by T-lymphocytes of PPMS patients, however, differ from effects observed in RRMS supporting the hypothesis that PPMS differs in some immunological aspects from RRMS. [source]

Mycobacterial heat shock protein-induced blood T lymphocytes subsets and cytokine pattern: Comparison of sarcoidosis with tuberculosis and healthy controls

Mitoxantrone treatment in multiple sclerosis induces TH2-type cytokines

ACTA NEUROLOGICA SCANDINAVICA, Issue 4 2010
A. Vogelgesang
Vogelgesang A, Rosenberg S, Skrzipek S, Bröker BM, Dressel A. Mitoxantrone treatment in multiple sclerosis induces TH2-type cytokines. Acta Neurol Scand: 2010: 122: 237,243. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objectives,,, Mitoxantrone is a cytotoxic drug with immune modulatory properties used in the treatment of progressive forms of multiple sclerosis (MS). We explored the effect of mitoxantrone treatment in MS patients on cytokine patterns induced in peripheral blood mononuclear cells (PBMC) and T-cell subsets ex vivo. Materials and methods,,, Blood was obtained before mitoxantrone infusion and 6, 12 and 18 days thereafter. Proliferation and prototypic TH1-, TH17- and TH2-type cytokines were determined following in vitro stimulation of PBMC, CD4+ and CD8+ T cells. In addition, a patient cohort receiving its first mitoxantrone treatment was cross-sectionally compared with a cohort of patients with more than 1 year of treatment. Results,,, Mitoxantrone treatment increased the ex vivo production of the TH2 cytokines interleukin-4 (IL-4; P < 0.05) and IL-5 (P < 0.001) in phytohemagglutinin-stimulated CD4+ T cells within 18 days of treatment. The cross-sectional study revealed that long-term treatment with mitoxantrone increased the inducibility of IL-4 and IL-5 secretion by PBMCs and CD4+ T cells even further. No significant changes were observed for interferon-,, tumour necrosis factor-,, IL-17 and IL-10. Mitoxantrone did not alter the proliferative capacity of ex vivo -stimulated T cells. Conclusion,,, Mitoxantrone treatment in MS enhances the inducibility of TH2-type cytokines, which may contribute to its beneficial effects in MS. [source]

Interferon- ,1b treatment modulates cytokines in patients with primary progressive multiple sclerosis

Differential immunomodulatory properties of Bifidobacterium logum strains: relevance to probiotic selection and clinical applications

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2007
M. Medina
Summary Modulation of host immunity is one of the proposed benefits of the consumption of probiotics. Nonetheless, comparative studies on the immunological properties that support the selection of strains of the same species for specific health benefits are limited. In this study, the ability of different strains of Bifidobacterium longum to induce cytokine production by peripheral blood mononuclear cells (PBMCs) has been evaluated. Live cells of all B. longum strains greatly stimulated regulatory cytokine interleukin (IL)-10 and proinflammatory cytokine tumour necrosis factor (TNF)-, production. Strains of the same species also induced specific cytokine patterns, suggesting that they could drive immune responses in different directions. The probiotic strain B. longum W11 stimulated strongly the production of T helper 1 (Th1) cytokines while B. longum NCIMB 8809 and BIF53 induced low levels of Th1 cytokines and high levels of IL-10. The effects of cell-surface components obtained by sonication of B. longum strains overall confirm the effects detected by stimulation of PBMCs with live cells, indicating that these components are important determinants of the immunomodulatory activity of B. longum. Genomic DNA of some strains stimulated the production of the Th1 and pro-inflammatory cytokines, interferon (IFN)-, and TNF-,, but not that of IL-10. None of the cell-free culture supernatants of the studied strains was able to induce TNF-, production, suggesting that the proinflammatory component of these strains is associated mainly with structural cell molecules. The results suggest that despite sharing certain features, some strains can perform a better functional role than others and their careful selection for therapeutic use is desirable. [source]

Mixed inflammatory/regulatory cytokine profile marked by simultaneous raise of interferon-, and interleukin-10 and low frequency of tumour necrosis factor-,+ monocytes are hallmarks of active human visceral Leishmaniasis due to Leishmania chagasi infection

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2006
V. Peruhype-Magalhães
Summary Considering the complexity of the immunological events triggered during active visceral Leishmaniasis (VL), the relevance of the segregation of the immune response during human VL into type 1 and type 2 still remains unclear. For this purpose, in individuals living in risk areas for VL, we have evaluated especially asymptomatic individuals and patients with active VL, the plasmatic levels of cytokines and reactive nitrogen species under ex vivo conditions. In addition, we have also performed an analysis of intracellular cytokine patterns of circulating leucocytes after short-term culture, particularly in the absence of antigenic-specific stimulation, in order to reflect dynamic events of immune response in vivo during Leishmania chagasi infection. Although asymptomatic individuals and non-infected subjects presented a similar immunological profile, an outstanding inflammatory/regulatory profile, based on higher plasmatic levels of cytokines such as interleukin (IL)-8, interferon (IFN)-,, tumour necrosis factor (TNF)-,, IL-6 and IL-10, was associated with clinical status observed in active VL. In this context, we hypothesize that IL-10, through its ability to inhibit anti-leishmanial macrophage activation, associated with the lower frequency of TNF-,+ monocytes and ordinary levels of nitrite and nitrate are the major mechanisms associated with disease onset. [source]