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  • 1
    Online Resource
    Online Resource
    Phlebotomine salivas inhibit immune inflammation-induced neutrophil migration via an autocrine DC-derived PGE2/IL-10 sequential pathway
    Oxford University Press (OUP) ; 2008
    In:  Journal of Leukocyte Biology Vol. 84, No. 1 ( 2008-07-01), p. 104-114
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 84, No. 1 ( 2008-07-01), p. 104-114
    Abstract: In the present study, we investigated whether saliva from Phlebotomus papatasi and Phlebotomus duboscqi inhibited antigen-induced neutrophil migration and the mechanisms involved in these effects. The pretreatment of immunized mice with salivary gland extracts (SGE) of both phlebotomines inhibited OVA challenge-induced neutrophil migration and release of the neutrophil chemotactic mediators, MIP-1α, TNF-α, and leukotriene B4 (LTB4). Furthermore, SGE treatment enhanced the production of anti-inflammatory mediators, IL-10 and PGE2. SGE treatments failed to inhibit neutrophil migration and MIP-1α and LTB4 production in IL-10−/− mice, also failing in mice treated with nonselective (indomethacin) or selective (rofecoxibe) cyclooxygenase (COX) inhibitors. COX inhibition resulted in diminished SGE-induced IL-10 production, and PGE2 release triggered by SGE remained increased in IL-10−/− mice, suggesting that prostanoids are acting through an IL-10-dependent mechanism. SGE treatments in vivo reduced the OVA-induced lymphoproliferation of spleen-derived cells. Further, the in vitro incubation of bone marrow-derived dendritic cells (DC) with SGE inhibited the proliferation of CD4+T cells from OVA-immunized mice, which was reversed by indomethacin and anti-IL-10 antibody treatments. Supporting these results, SGE induced the production of PGE2 and IL-10 by DC, which were blocked by COX inhibition. These effects were associated with the reduction of DC-membrane expression of MHC-II and CD86 by SGE treatment. Altogether, the results showed that Phlebotomine saliva inhibits immune inflammation-induced neutrophil migration by an autocrine DC sequential production of PGE2/IL-10, suggesting that the saliva constituents might be promising therapeutic molecules to target immune inflammatory diseases.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    URL: Article
    DOI: 10.1189/jlb.1107797
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2008
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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  • 2
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    Therapeutic Treatment of Arthritic Mice with 15-Deoxy Δ 12,14 -Prostaglandin J 2 (15d-PGJ 2 ) Ameliorates Disease through the Suppression of Th17 Cells and the Induction of CD4 + CD25 − FOXP3 + Cells
    Hindawi Limited ; 2016
    In:  Mediators of Inflammation Vol. 2016 ( 2016), p. 1-13
    Details
    In: Mediators of Inflammation, Hindawi Limited, Vol. 2016 ( 2016), p. 1-13
    Abstract: The prostaglandin, 15-deoxy Δ 12,14 -prostaglandin J 2 (15d-PGJ 2 ), is a lipid mediator that plays an important role in the control of chronic inflammatory disease. However, the role of prostanoid in rheumatoid arthritis (RA) is not well determined. We demonstrated the therapeutic effect of 15d-PGJ 2 in an experimental model of arthritis. Daily administration of 15d-PGJ 2 attenuated the severity of CIA, reducing the clinical score, pain, and edema. 15d-PGJ 2 treatment was associated with a marked reduction in joint levels of proinflammatory cytokines. Although the mRNA expression of ROR- γ t was profoundly reduced, FOXP3 was enhanced in draining lymph node cells from 15d-PGJ 2 -treated arthritic mice. The specific and polyclonal CD4 + Th17 cell responses were limited during the addition of prostaglandin to cell culture. Moreover, in vitro 15d-PGJ 2 increased the expression of FOXP3, GITR, and CTLA-4 in the CD4 + CD25 − population, suggesting the induction of Tregs on conventional T cells. Prostanoid addition to CD4 + CD25 − cells selectively suppressed Th17 differentiation and promoted the enhancement of FOXP3 under polarization conditions. Thus, 15d-PGJ 2 ameliorated symptoms of collagen-induced arthritis by regulating Th17 differentiation, concomitant with the induction of Tregs, and, consequently, protected mice from diseases aggravation. Altogether, these results indicate that 15d-PGJ 2 may represent a potential therapeutic strategy in RA.
    Type of Medium: Online Resource
    ISSN: 0962-9351 , 1466-1861
    URL: Article
    DOI: 10.1155/2016/9626427
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2016
    detail.hit.zdb_id: 2008065-7
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  • 3
    Online Resource
    Online Resource
    Nucleosides from Phlebotomus papatasi Salivary Gland Ameliorate Murine Collagen-Induced Arthritis by Impairing Dendritic Cell Functions
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 187, No. 8 ( 2011-10-15), p. 4347-4359
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 187, No. 8 ( 2011-10-15), p. 4347-4359
    Abstract: Among several pharmacological compounds, Phlebotomine saliva contains substances with anti-inflammatory properties. In this article, we demonstrated the therapeutic activity of salivary gland extract (SGE) of Phlebotomus papatasi in an experimental model of arthritis (collagen-induced arthritis [CIA]) and identified the constituents responsible for such activity. Daily administration of SGE, initiated at disease onset, attenuated the severity of CIA, reducing the joint lesion and proinflammatory cytokine release. In vitro incubation of dendritic cells (DCs) with SGE limited specific CD4+ Th17 cell response. We identified adenosine (ADO) and 5′AMP as the major salivary molecules responsible for anti-inflammatory activities. Pharmacologic inhibition of ADO A2A receptor or enzymatic catabolism of salivary nucleosides reversed the SGE-induced immunosuppressive effect. Importantly, CD73 (ecto-5′-nucleotidase enzyme) is expressed on DC surface during stage of activation, suggesting that ADO is also generated by 5′AMP metabolism. Moreover, both nucleosides mimicked SGE-induced anti-inflammatory activity upon DC function in vitro and attenuated establishment of CIA in vivo. We reveal that ADO and 5′AMP are present in pharmacological amounts in P. papatasi saliva and act preferentially on DC function, consequently reducing Th17 subset activation and suppressing the autoimmune response. Thus, it is plausible that these constituents might be promising therapeutic molecules to target immune inflammatory diseases.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1003404
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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  • 4
    Online Resource
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    15d-PGJ2 ameliorates collagen-induced arthritis by convergence of Th17 to induced-Tregs (83.1)
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 184, No. 1_Supplement ( 2010-04-01), p. 83.1-83.1
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1_Supplement ( 2010-04-01), p. 83.1-83.1
    Abstract: Regulatory T cells (Treg) are CD4+T subtype cells with a critical role in inhibiting autoimmunity. Several works reported efficacy therapeutic of 15d-PGJ2 in autoimmune models as well in vitro is able to generate the differentiation of naïve T lymphocytes to the regulatory profile. However, this prostanoid use and its interrelationship with Tregs during the arthritis rheumatoid are unknown. In view of a therapeutic perspective, we investigate the potential role of 15d-PGJ2 in a model of collagen-induced arthritis (CIA) and its interplay with Tregs-induced anti-inflammatory mechanism. CIA was elicited in DBA male mice by collagen-emulsion injection and then treated with 15-PGJ2 daily during 7 days. 15d-PGJ2 administration at the disease onset attenuated the severity of CIA, reducing clinical score, pain and edema. Furthermore, while the mRNA expression of ROR-γt was reduced, FOXP3 expression was up-regulated in draining lymph nodes cells from 15d-PGJ2-treated mice. In vitro, 15-PGJ2 increased the expression of FOXP3, GITR and CTLA-4, Tregs makers, on CD4+CD25- population, suggesting the induction of Tregs on effector cells. Coculture of Th17 cells with 15d-PGJ2-induced Treg reduced significantly the IL-17 production by collagen and α-CD3 stimuli whereas IL-10 production was enhanced. 15d-PGJ2 converge Th17 lymphocytes to regulatory profile, reducing the number of pathogenic T cells and consequently suppressing the inflammatory immune response. FAPEMIG 097/09
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.184.Supp.83.1
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
    detail.hit.zdb_id: 1475085-5
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