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  • 1
    Online Resource
    Online Resource
    Thymic Stromal Lymphopoietin Enhances Th2/Th22 and Reduces IL-17A in Protease-Allergen-Induced Airways Inflammation
    Hindawi Limited ; 2013
    In:  ISRN Allergy Vol. 2013 ( 2013-02-07), p. 1-14
    Details
    In: ISRN Allergy, Hindawi Limited, Vol. 2013 ( 2013-02-07), p. 1-14
    Abstract: Background . Thymic stromal lymphopoietin (TSLP) is induced in allergic skin and lung inflammation in man and mice. Methods . Allergic lung inflammation induced by two proteases allergens HDM and papain and a classical allergen ovalbumin was evaluated in vivo in mice deficient for TSLPR. Eosinophil recruitment, Th2 and Th17 cytokine and chemokine levels were determined in bronchoalveolar lavage fluid, lung homogenates and lung mononuclear cells ex vivo . Results . Here we report that mice challenged with house dust mite extract or papain in the absence of TSLPR have a drastic reduction of allergic inflammation with diminished eosinophil recruitment in BAL and lung and reduced mucus overproduction. TSLPR deficient DCs displayed diminished OVA antigen uptake and reduced capacity to activate antigen specific T cells. TSLPR deficient mice had diminished proinflammatory IL-1 β , IL-13, and IL-33 chemokines production, while IL-17A, IL-12p40 and IL-10 were increased. Together with impaired Th2 cytokines, IL-17A expressing TCR β + T cells were increased, while IL-22 expressing CD4 + T cells were diminished in the lung. Conclusion . Therefore, TSLPR signaling is required for the development of both Th2 and Th22 responses and may restrain IL-17A. TSLP may mediate its effects in part by increasing allergen uptake and processing by DCs resulting in an exacerbated asthma.
    Type of Medium: Online Resource
    ISSN: 2090-553X
    URL: Article
    DOI: 10.1155/2013/971036
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2013
    detail.hit.zdb_id: 2616877-7
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  • 2
    Online Resource
    Online Resource
    Neutrophil Inhibitory Factor Selectively Inhibits the Endothelium-Driven Transmigration of Eosinophils In Vitro and Airway Eosinophilia in OVA-Induced Allergic Lung Inflammation
    Hindawi Limited ; 2012
    In:  Journal of Allergy Vol. 2012 ( 2012-12-04), p. 1-10
    Details
    In: Journal of Allergy, Hindawi Limited, Vol. 2012 ( 2012-12-04), p. 1-10
    Abstract: Leukocyte adhesion molecules are involved in cell recruitment in an allergic airway response and therefore provide a target for pharmaceutical intervention. Neutrophil inhibitory factor (NIF), derived from canine hookworm ( Ancylostoma caninum ), binds selectively and competes with the A-domain of CD11b for binding to ICAM-1. The effect of recombinant NIF was investigated. Intranasal administration of rNIF reduced pulmonary eosinophilic infiltration, goblet cell hyperplasia, and Th 2 cytokine production in OVA-sensitized mice. In vitro , transendothelial migration of human blood eosinophils across IL-4-activated umbilical vein endothelial cell (HUVEC) monolayers was inhibited by rNIF (IC 50 : 4.6 ± 2.6  nM; mean ± SEM), but not across TNF or IL-1-activated HUVEC monolayers. Treatment of eosinophils with rNIF together with mAb 60.1 directed against CD11b or mAb 107 directed against the metal ion-dependent adhesion site (MIDAS) of the CD11b A-domain resulted in no further inhibition of transendothelial migration suggesting shared functional epitopes. In contrast, rNIF increased the inhibitory effect of blocking mAbs against CD18, CD11a, and VLA-4. Together, we show that rNIF, a selective antagonist of the A-domain of CD11b, has a prominent inhibitory effect on eosinophil transendothelial migration in vitro , which is congruent to the in vivo inhibition of OVA-induced allergic lung inflammation.
    Type of Medium: Online Resource
    ISSN: 1687-9783 , 1687-9791
    URL: Article
    DOI: 10.1155/2012/245909
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2012
    detail.hit.zdb_id: 2571416-8
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  • 3
    Online Resource
    Online Resource
    Induction of NLRP3 Inflammasome Activation by Heme in Human Endothelial Cells
    Hindawi Limited ; 2018
    In:  Oxidative Medicine and Cellular Longevity Vol. 2018 ( 2018), p. 1-14
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2018 ( 2018), p. 1-14
    Abstract: Hemolytic or hemorrhagic episodes are often associated with inflammation even when infectious agents are absent suggesting that red blood cells (RBCs) release damage-associated molecular patterns (DAMPs). DAMPs activate immune and nonimmune cells through pattern recognition receptors. Heme, released from RBCs, is a DAMP and induces IL-1 β production through the activation of the nucleotide-binding domain and leucine-rich repeat-containing family and pyrin domain containing 3 (NLRP3) in macrophages; however, other cellular targets of heme-mediated inflammasome activation were not investigated. Because of their location, endothelial cells can be largely exposed to RBC-derived DAMPs; therefore, we investigated whether heme and other hemoglobin- (Hb-) derived species induce NLRP3 inflammasome activation in these cells. We found that heme upregulated NLRP3 expression and induced active IL-1 β production in human umbilical vein endothelial cells (HUVECs). LPS priming largely amplified the heme-mediated production of IL-1 β . Heme administration into C57BL/6 mice induced caspase-1 activation and cleavage of IL-1 β which was not observed in NLRP3 −/− mice. Unfettered production of reactive oxygen species played a critical role in heme-mediated NLRP3 activation. Activation of NLRP3 by heme required structural integrity of the heme molecule, as neither protoporphyrin IX nor iron-induced IL-1 β production. Neither naive nor oxidized forms of Hb were able to induce IL-1 β production in HUVECs. Our results identified endothelial cells as a target of heme-mediated NLRP3 activation that can contribute to the inflammation triggered by sterile hemolysis. Thus, understanding the characteristics and cellular counterparts of RBC-derived DAMPs might allow us to identify new therapeutic targets for hemolytic diseases.
    Type of Medium: Online Resource
    ISSN: 1942-0900 , 1942-0994
    URL: Article
    DOI: 10.1155/2018/4310816
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2018
    detail.hit.zdb_id: 2455981-7
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  • 4
    Online Resource
    Online Resource
    Effects of Nintedanib in an Animal Model of Liver Fibrosis
    Hindawi Limited ; 2020
    In:  BioMed Research International Vol. 2020 ( 2020-03-31), p. 1-9
    Details
    In: BioMed Research International, Hindawi Limited, Vol. 2020 ( 2020-03-31), p. 1-9
    Abstract: Systemic sclerosis can affect multiple internal organs, including the liver and lungs. Nintedanib, an antifibrotic approved for treatment of interstitial lung disease associated with systemic sclerosis, may have activity outside of the lungs. This study explored the effect of preventive and therapeutic nintedanib treatment in a 3-week carbon tetrachloride (CCL 4 )-induced (500 mg/kg/day twice weekly for 3 weeks) model of hepatic inflammation and fibrosis in C57Bl/6 mice (aged 8 weeks, n = 5 per group). Mice also received nintedanib (30 or 60 mg/kg/day) either each day for 21 days (preventive treatment) or from day 7 or day 14 (therapeutic treatment). Preventive nintedanib treatment at both doses significantly reduced CCL 4 -induced increases in myeloperoxidase ( p 〈 0.01 ), hepatic collagen ( p 〈 0.001 ), and interleukin (IL)-6 ( p 〈 0.01 ) in the liver. Nintedanib also significantly reduced hepatic necrosis ( p 〈 0.01 and p 〈 0.05 ), inflammation ( p 〈 0.001 and p 〈 0.05 ), fibrosis ( p 〈 0.001 and p 〈 0.05 ) and IL-1 β ( p 〈 0.05 and p 〈 0.001 ) at both 30 and 60 mg/kg/day, respectively. Therapeutic treatment with nintedanib at 30 and 60 mg/kg/day significantly reduced CCL 4 -induced serum alanine aminotransferase from day 7 ( p 〈 0.05 and p 〈 0.001 ) and day 14 ( p 〈 0.01 and p 〈 0.05 ), respectively. Increases in tissue inhibitor of metalloproteinase-1 were significantly reduced by nintedanib at 60 mg/kg/day from day 7 only ( p 〈 0.001 ), and nintedanib completely blocked elevation of IL-6 and IL-1 β levels regardless of dose or start of treatment ( p 〈 0.05 – p 〈 0.001 ). In both the preventive and therapeutic treatment schedules of the study, nintedanib treatment was beneficial in attenuating CCL 4 -induced pathology and reducing hepatic injury, inflammation, and fibrosis, demonstrating that nintedanib has antifibrotic and anti-inflammatory activity outside of the lungs.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    URL: Article
    DOI: 10.1155/2020/3867198
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2698540-8
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  • 5
    Online Resource
    Online Resource
    Correction of the TNF-LTα-Deficient Phenotype by Bone Marrow Transplantation
    Hindawi Limited ; 1998
    In:  Developmental Immunology Vol. 6, No. 3-4 ( 1998), p. 253-260
    Details
    In: Developmental Immunology, Hindawi Limited, Vol. 6, No. 3-4 ( 1998), p. 253-260
    Type of Medium: Online Resource
    ISSN: 1044-6672
    URL: Article
    DOI: 10.1155/1998/76963
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 1998
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