المؤلفون: Barbour, S. E.

مصطلحات موضوعية: 639.8, Aquaculture

الإتاحة: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.350765Test

المؤلفون: Lei, X., Zhang, S., Emani, B., Barbour, S. E., Ramanadham, S.

المصدر: Diabetes, Obesity and Metabolism ; volume 12, issue s2, page 93-98 ; ISSN 1462-8902 1463-1326

الوصف: Endoplasmic reticulum (ER) stress is becoming recognized as an important contributing factor in various diseases, including diabetes mellitus. Prolonged ER stress can cause β ‐cell apoptosis; however, the underlying mechanism(s) that contribute to this process are not well understood. Early reports suggested that arachidonic acid metabolites and a Ca 2+ ‐independent phospholipase A 2 (iPLA 2 ) activity play a role in β ‐cell apoptosis. The PLA 2 family of enzymes catalyse the hydrolysis of the sn ‐2 substituent (i.e. arachidonic acid) of membrane phospholipids. In light of our findings that the pancreatic islet β ‐cells are enriched in arachidonate‐containing phospholipids and express the group VIA iPLA 2 β , we considered the possibility that iPLA 2 β participates in ER stress‐induced β ‐cell apoptosis. Our work revealed a novel mechanism, involving ceramide generation and triggering of mitochondrial abnormalities, by which iPLA 2 β participates in the β ‐cell apoptosis process. Here, we review our evidence linking ER stress, β ‐cell apoptosis and iPLA 2 β . Continued studies in this area will increase our understanding of the contribution of iPLA 2 β to the evolution of diabetes mellitus and will further our knowledge of factors that influence β ‐cell health in diabetes mellitus and identify potential targets for future therapeutic interventions to prevent β ‐cell death.

الإتاحة: https://doi.org/10.1111/j.1463-1326.2010.01270.xTest

المؤلفون: Kikuchi, T., Hahn, C. L., Tanaka, S., Barbour, S. E., Schenkein, H. A., Tew, J. G.

المصدر: Infection and Immunity ; volume 72, issue 9, page 5089-5096 ; ISSN 0019-9567 1098-5522

الوصف: Human immunoglobulin G2 (IgG2) responses are gamma interferon (IFN-γ) dependent, and monocyte-derived dendritic cells (mDCs) promote IgG2 production. DCs spontaneously emerge from monocytes in cultures prepared from localized aggressive periodontitis (LagP) patients, and these patients have high levels of IgG2 that is reactive with Actinobacillus actinomycetemcomitans . These results prompted the hypothesis that an interaction between mDCs and A. actinomycetemcomitans promotes IFN-γ production, and IFN-γ is known to promote both immunopathology and protective IgG2. A. actinomycetemcomitans induced mDCs to produce interleukin-12 (IL-12), and the addition of A. actinomycetemcomitans and DCs to cultured peripheral blood lymphocytes elicited high levels of IFN-γ within just 24 h. In contrast, IL-4 was not detectable although DC-derived IL-10 production was apparent. A. actinomycetemcomitans -stimulated macrophages prepared from the same monocytes lacked the ability to induce IL-12 or IFN-γ responses. NK cells of the innate immune system were the primary source of this early IFN-γ, although CD8 T cells also contributed some. The NK cell-derived IFN-γ was IL-12 dependent, and A. actinomycetemcomitans -DC interactions were Toll-like receptor 4 dependent. A. actinomycetemcomitans and A. actinomycetemcomitans lipopolysaccharide (LPS) were more potent than Escherichia coli and E. coli LPS in the ability to induce DC IL-12 and IFN-γ. The ability of A. actinomycetemcomitans -stimulated DCs to induce NK cells to rapidly produce IFN-γ in the absence of detectable IL-4 suggests their potential for skewing responses toward Th1. This may help explain the presence of Th1-associated cytokines in gingival crevicular fluid (GCF) from LagP patients and the high levels of IgG2 in their serum and GCF that is reactive with A. actinomycetemcomitans .

الإتاحة: https://doi.org/10.1128/iai.72.9.5089-5096.2004Test

المؤلفون: Kikuchi, T., El Shikh, M. M., El Sayed, R. M., Purkall, D. B., Elaasser, M. M., Sarraf, A., Barbour, S. E., Schenkein, H. A., Tew, J. G.

المصدر: Journal of Periodontal Research ; volume 45, issue 6, page 720-730 ; ISSN 0022-3484

الإتاحة: https://doi.org/10.1111/j.1600-0765.2010.01292.xTest

المؤلفون: Rufail, M. L., Schenkein, H. A., Koertge, T. E., Best, A. M., Barbour, S. E., Tew, J. G., Van Antwerpen, R.

المصدر: Journal of Periodontal Research ; volume 42, issue 6, page 495-502 ; ISSN 0022-3484 1600-0765

الوصف: Background and Objective: Certain types of chronic infection increase the plasma level of very‐low‐density lipoprotein, leading to formation of the particularly atherogenic low‐density lipoprotein subclass, small dense low‐density lipoprotein. In the present study, we examined whether aggressive forms of periodontis are associated with these atherogenic lipoprotein parameters. Material and Methods: Twelve healthy control subjects without periodontitis, 12 subjects with localized aggressive periodontitis and 12 subjects with generalized aggressive periodontitis were studied. Lipoprotein subclass levels were determined using nuclear magnetic resonance methodology. Results: Healthy control subjects, localized aggressive periodontitis subjects and generalized aggressive periodontitis subjects had progressively higher plasma levels of very‐low‐density lipoprotein and progressively smaller average low‐density lipoprotein size ( p < 0.05, one‐way analysis of variance). In pairwise comparisons, differences were only significant between healthy controls and generalized aggressive periodontitis subjects ( p < 0.05, Tukey's post test). After adjustment for body mass index, the mean periodontal pocket depth correlated positively with plasma very‐low‐density lipoprotein levels ( p = 0.047). Very‐low‐density lipoprotein concentrations correlated positively with small dense low‐density lipoprotein levels and negatively with average low‐density lipoprotein size. Prevalence of the atherogenic lipoprotein pattern‐B in healthy controls, localized aggressive periodontitis subjects and generalized aggressive periodontitis subjects was 8.3%, 33.3% and 66.6%, respectively. Conclusion: These results indicate that periodontal infection is associated with elevated plasma levels of atherogenic lipoprotein species. This association may account for the increased risk of periodontitis patients for cardiovascular disease.

الإتاحة: https://doi.org/10.1111/j.1600-0765.2007.00973.xTest

المؤلفون: Shin, C. R., Moores, J., Best, A. M., Tew, J. G., Schenkein, H. A., Barbour, S. E.

المصدر: Journal of Periodontal Research ; volume 42, issue 3, page 202-211 ; ISSN 0022-3484 1600-0765

الوصف: Background and Objective: Platelet‐activating factor is elevated in localized aggressive periodontitis. We previously demonstrated that the elevated level of platelet‐activating factor in localized aggressive periodontitis is at least partially attributable to low levels of platelet‐activating factor acetylhydrolase, the enzyme that catabolizes platelet‐activating factor. The objective of this study was to determine if platelet‐activating factor synthesis was also elevated in localized aggressive periodontitis. To test this, platelet‐activating factor synthesis was quantified in the monocytes and polymorphonuclear neutrophils of periodontally healthy patients and of subjects with localized aggressive periodontitis. Material and Methods: Cells were labeled with [ 3 H]acetate and treated with vehicle or stimulated with calcium ionophore A23187. Platelet‐activating factor was extracted and quantified by scintillation counting. Results: For both subject groups, resting monocytes and polymorphonuclear neutrophils produced platelet‐activating factor, and calcium ionophore A23187 stimulated platelet‐activating factor production in both cell types. However, calcium ionophore A23187‐activated monocytes from subjects with localized aggressive periodontitis produced less platelet‐activating factor than did activated periodontally healthy monocytes ( p < 0.0001), suggesting an aberrant calcium ionophore A23187 response in monocytes from subjects with localized aggressive periodontitis. Indeed, when the data were expressed as fold induction of platelet‐activating factor synthesis in response to calcium ionophore A23187, monocytes from subjects with localized aggressive periodontitis exhibited only a fourfold increase in platelet‐activating factor synthesis, whereas calcium ionophore A23187‐stimulated monocytes from periodontally healthy, chronic periodontitis and generalized aggressive periodontitis subjects produced ≈ 12 times more platelet‐activating factor than did resting monocytes. In contrast, both resting and ...

الإتاحة: https://doi.org/10.1111/j.1600-0765.2006.00933.xTest

المؤلفون: Tanaka, S., Fakher, M., Barbour, S. E., Schenkein, H. A., Tew, J. G.

المصدر: Journal of Periodontal Research ; volume 41, issue 1, page 1-9 ; ISSN 0022-3484 1600-0765

الوصف: Objective: High levels of serum anti‐ Actinobacillus actinomycetemcomitans immunoglobulin G (IgG) correlate with reduced extent and severity of periodontal disease and the present study was undertaken to begin testing the hypothesis that proinflammatory cytokines are important in the induction of optimal anti‐ A. actinomycetemcomitans IgG responses. Background: Studies with pokeweed mitogen indicate that interleukin‐1α (IL‐1α) and IL‐1β are necessary for optimal IgG1 and IgG2 production and that prostaglandin E 2 (PGE 2 ) and interferon‐γ (IFN‐γ) selectively promote IgG2, which is a major component of the anti‐ A. actinomycetemcomitans response in vivo . The pokeweed mitogen results suggest that these proinflammatory cytokines would also be necessary for optimal production of IgG specific for A. actinomycetemcomitans . Methods: Peripheral blood mononuclear cells from A. actinomycetemcomitans ‐seropositive subjects with localized aggressive periodontitis were stimulated with A. actinomycetemcomitans in immune complexes capable of binding follicular dendritic cells that participate in the induction of recall responses in vivo . Cultures were manipulated with anti‐IL‐1α, anti‐IL‐1β, anti‐IFN‐γ, anti‐IL‐12, anti‐CD21, indomethacin, and PGE 2 . Actinobacillus actinomycetemcomitans specific IgG production was monitored by enzyme‐linked immunosorbent assay (ELISA). Results: Addition of follicular dendritic cells to peripheral blood mononuclear cells cultures resulted in follicular dendritic cell‐lymphocyte clusters and increased anti‐ A. actinomycetemcomitans IgG responses (3–40‐fold increases) compared with controls lacking follicular dendritic cells. Anti‐IL‐1α, anti‐IL‐1β, anti‐IFN‐γ, anti‐IL‐12, anti‐CD21 and indomethacin suppressed anti‐ A. actinomycetemcomitans IgG production by half or more. PGE 2 restored IgG responses suppressed by indomethacin. Conclusions: The cytokines IL‐1α, IL‐1β, IFN‐γ, IL‐12, and PGE 2 were all necessary for optimal production of human anti‐ A. actinomycetemcomitans and the need for ...

الإتاحة: https://doi.org/10.1111/j.1600-0765.2005.00829.xTest

المؤلفون: Kikuchi, T., El Shikh, M. M., El Sayed, R. M., Purkall, D. B., Elaasser, M. M., Sarraf, A., Barbour, S. E., Schenkein, H. A., Tew, J. G.

المصدر: Journal of Periodontal Research; Dec2010, Vol. 45 Issue 6, p720-730, 11p

مصطلحات موضوعية: CELL physiology, CYTOKINES, ENZYME-linked immunosorbent assay, FLOW cytometry, INTERLEUKINS, LIPOPROTEINS, RESEARCH

مستخلص: Kikuchi T, El Shikh MM, El Sayed RM, Purkall DB, Elaasser MM, Sarraf A, Barbour SE, Schenkein HA, Tew JG. Anti-phosphorylcholine opsonized low-density lipoprotein promotes rapid production of proinflammatory cytokines by dendritic cells and natural killer cells. J Periodont Res 2010; 45: 720-730. © 2010 John Wiley & Sons A/S Epidemiological and animal studies suggest that periodontal infections increase atherosclerosis risk. Periodontitis patients have elevated levels of anti-phosphorylcholine (anti-PC) reactive not only with numerous periodontal organisms but also with minimally modified low-density lipoprotein (mmLDL). Dendritic cells (DCs) reside in arterial walls and accumulate in atherosclerotic lesions. The ability of anti-PC to bind mmLDL prompted the hypothesis that opsonized mmLDL would stimulate DCs and enhance the production of proinflammatory cytokines that promote atherogenic plaque development. Monocyte-derived DCs (mDCs) were generated using granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-4, then stimulated with mmLDL or with anti-PC-opsonized mmLDL. The anti-PC effect was determined using flow cytometry, cofocal microscopy and cytokine assays. The production of CD83, IL-12p35 mRNA, IL-12p40 mRNA, IL-12p70 and IL-10 by DCs was monitored. Dendritic cells stimulated with mmLDL expressed little CD83 and produced little IL-12p70. However, anti-PC-opsonized mmLDL enhanced DC maturation, as indicated by upregulated CD83 and rapid (≤ 48 h) production of IL-12p70 if a source of interferon-γ (IFN-γ) was available. In leukocyte cultures, natural killer (NK) cells rapidly produced IFN-γ (≤ 48 h) when interacting with IL-12-producing DCs activated by anti-PC-opsonized mmLDL. Moreover, IFN-γ promoted DC IL-12 responses that were further augmented when mmLDL was opsonized with anti-PC. Minimally modified LDL-stimulated DCs and NK cells were mutually stimulatory, with DC IL-12p70 needed by NK cells and with NK cell IFN-γ needed by DCs. Moreover, production of these proinflammatory cytokines was markedly enhanced when LDL was opsonized by anti-PC. In short, the data suggest that the elevated anti-PC levels in periodontitis patients could promote a mechanism that facilitates atherosclerosis. [ABSTRACT FROM AUTHOR]

: Copyright of Journal of Periodontal Research is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Lei, X., Zhang, S., Emani, B., Barbour, S. E., Ramanadham, S.

المصدر: Diabetes, Obesity & Metabolism; Oct2010 Supplement, p93-98, 6p, 1 Diagram

مستخلص: Endoplasmic reticulum (ER) stress is becoming recognized as an important contributing factor in various diseases, including diabetes mellitus. Prolonged ER stress can cause β-cell apoptosis; however, the underlying mechanism(s) that contribute to this process are not well understood. Early reports suggested that arachidonic acid metabolites and a Ca²⁺-independent phospholipase A2 (iPLA2) activity play a role in β-cell apoptosis. The PLA2 family of enzymes catalyse the hydrolysis of the sn-2 substituent (i.e. arachidonic acid) of membrane phospholipids. In light of our findings that the pancreatic islet β-cells are enriched in arachidonate-containing phospholipids and express the group VIA iPLA2β, we considered the possibility that iPLA2β participates in ER stress-induced β-cell apoptosis. Our work revealed a novel mechanism, involving ceramide generation and triggering of mitochondrial abnormalities, by which iPLA2β participates in the β-cell apoptosis process. Here, we review our evidence linking ER stress, β-cell apoptosis and iPLA2β. Continued studies in this area will increase our understanding of the contribution of iPLA2β to the evolution of diabetes mellitus and will further our knowledge of factors that influence β-cell health in diabetes mellitus and identify potential targets for future therapeutic interventions to prevent β-cell death. [ABSTRACT FROM AUTHOR]

: Copyright of Diabetes, Obesity & Metabolism is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Tanaka, S., Fakher, M., Barbour, S. E., Schenkein, H. A., Tew, J. G.

المصدر: Journal of Periodontal Research; Feb2006, Vol. 41 Issue 1, p1-9, 9p, 5 Graphs

مصطلحات موضوعية: CYTOKINES, CELLULAR immunity, IMMUNOREGULATION, ACTINOBACILLUS, BRUCELLACEAE, IMMUNOGLOBULIN G, PERIODONTAL disease, PERIODONTICS, GINGIVAL diseases

مستخلص: Objective: High levels of serum anti- Actinobacillus actinomycetemcomitans immunoglobulin G (IgG) correlate with reduced extent and severity of periodontal disease and the present study was undertaken to begin testing the hypothesis that proinflammatory cytokines are important in the induction of optimal anti- A. actinomycetemcomitans IgG responses. Background: Studies with pokeweed mitogen indicate that interleukin-1α (IL-1α) and IL-1β are necessary for optimal IgG1 and IgG2 production and that prostaglandin E2 (PGE2) and interferon-γ (IFN-γ) selectively promote IgG2, which is a major component of the anti- A. actinomycetemcomitans response in vivo. The pokeweed mitogen results suggest that these proinflammatory cytokines would also be necessary for optimal production of IgG specific for A. actinomycetemcomitans. Methods: Peripheral blood mononuclear cells from A. actinomycetemcomitans-seropositive subjects with localized aggressive periodontitis were stimulated with A. actinomycetemcomitans in immune complexes capable of binding follicular dendritic cells that participate in the induction of recall responses in vivo. Cultures were manipulated with anti-IL-1α, anti-IL-1β, anti-IFN-γ, anti-IL-12, anti-CD21, indomethacin, and PGE2. Actinobacillus actinomycetemcomitans specific IgG production was monitored by enzyme-linked immunosorbent assay (ELISA). Results: Addition of follicular dendritic cells to peripheral blood mononuclear cells cultures resulted in follicular dendritic cell-lymphocyte clusters and increased anti- A. actinomycetemcomitans IgG responses (3–40-fold increases) compared with controls lacking follicular dendritic cells. Anti-IL-1α, anti-IL-1β, anti-IFN-γ, anti-IL-12, anti-CD21 and indomethacin suppressed anti- A. actinomycetemcomitans IgG production by half or more. PGE2 restored IgG responses suppressed by indomethacin. Conclusions: The cytokines IL-1α, IL-1β, IFN-γ, IL-12, and PGE2 were all necessary for optimal production of human anti- A. actinomycetemcomitans and the need for proinflammatory cytokines including the T helper 1 (Th1) cytokines is consistent with a response with a significant IgG2 component. [ABSTRACT FROM AUTHOR]

: Copyright of Journal of Periodontal Research is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)