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- Gao, H., et al.
(författare)
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Estrogen attenuates vascular expression of inflammation associated genes and adhesion of monocytes to endothelial cells
- 2006
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Ingår i: Inflammation Research. - : Springer Science and Business Media LLC. - 1420-908X .- 1023-3830. ; 55:8, s. 349-353
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Investigate effects of estrogen at gene expression and functional levels in vascular wall cells treated with bacterial lipopolysaccharide (LPS). Materials and methods: Aortic segments from ovariectomized mice were treated with LPS for 24 h in the absence or presence of 17 beta-estradiol (E-2). Gene activity was determined by Affymetrix microarray analysis and real-time RTPCR. Adhesion of [H-3]-thymidine labelled human THP-1 monocytes to mouse bEnd.3 endothelial cells was determined by measuring radioactivity of DNA from co-culture homogenates. Results: Analysis of global gene expression profiles revealed that 10 nM E-2 attenuates LPS-induced (10 ng/ml) expression of genes coding for well-known acute-phase proteins, such as alpha-trypsin inhibitor heavy chain 4, serum amyloid A3 and lipocalin 2. The E-2-induced down-regulation of these three genes observed by microarray was confirmed by realtime RT-PCR. Treatment with 500ng/ml LPS increased adhesion of monocytes to endothelial cells more than two fold. Importantly, LPS-induced monocyte adhesion was fully prevented by 50nM E-2. Conclusion: Estrogen reduces expression of acute-phase protein genes and inhibits LPS-induced moncocyte adhesion to endothelial cells, suggesting that estrogen might have a vasculoprotective effect via this mechanism.
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- Jönsson, Daniel, et al.
(författare)
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LPS induces GROalpha chemokine production via NF-kappaB in oral fibroblasts.
- 2009
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Ingår i: Inflammation Research. - : Springer Science and Business Media LLC. - 1420-908X .- 1023-3830. ; 58:11, s. 791-796
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Tidskriftsartikel (refereegranskat)abstract
- Objective and design Chemotaxis of neutrophils from blood to the inflammation process plays an important role in development of periodontal inflammation. The novel chemokine GRO alpha, also named CXCL1, is a strong chemoattractant for neutrophils. Data on production and regulation of GRO alpha by oral fibroblasts have not previously been presented. Materials and methods GRO alpha mRNA and protein levels were determined in human periodontal ligament cells and mouse gingival fibroblasts by quantitative real-time PCR and ELISA. Results We disclose that both human periodontal ligament cells and mouse gingival fibroblasts produce GRO alpha in response to LPS stimulation. Stimulation with LPS for 24 h increased both mRNA for GRO alpha and GRO alpha protein. The steroid hormone estrogen had no effect on LPS-induced GRO alpha mRNA expression. Treatment with the glucocorticoid dexamethasone attenuated LPS-induced GRO alpha production, and the NF-kappa B blocker MG 132 fully prevented LPS-induced GRO alpha. Conclusions Oral fibroblasts respond to LPS stimulation by increasing GRO alpha production via the transcription factor NF-kappa B, suggesting that this mechanism may be involved in development of periodontal inflammation.
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- Jönsson, Daniel, et al.
(författare)
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LPS induces GROα chemokine production via NFκB in oral fibroblasts
- 2009
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Ingår i: Inflammation Research. - : Springer. - 1023-3830 .- 1420-908X. ; 11:58, s. 791-796
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE AND DESIGN: Chemotaxis of neutrophils from blood to the inflammation process plays an important role in development of periodontal inflammation. The novel chemokine GROalpha, also named CXCL1, is a strong chemoattractant for neutrophils. Data on production and regulation of GROalpha by oral fibroblasts have not previously been presented. MATERIALS AND METHODS: GROalpha mRNA and protein levels were determined in human periodontal ligament cells and mouse gingival fibroblasts by quantitative real-time PCR and ELISA. RESULTS: We disclose that both human periodontal ligament cells and mouse gingival fibroblasts produce GROalpha in response to LPS stimulation. Stimulation with LPS for 24 h increased both mRNA for GROalpha and GROalpha protein. The steroid hormone estrogen had no effect on LPS-induced GROalpha mRNA expression. Treatment with the glucocorticoid dexamethasone attenuated LPS-induced GROalpha production, and the NF-kappaB blocker MG 132 fully prevented LPS-induced GROalpha. CONCLUSIONS: Oral fibroblasts respond to LPS stimulation by increasing GROalpha production via the transcription factor NF-kappaB, suggesting that this mechanism may be involved in development of periodontal inflammation.
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- Mangell, Peter, et al.
(författare)
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Critical role of P-selectin-dependent leukocyte recruitment in endotoxin-induced intestinal barrier dysfunction in mice.
- 2007
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Ingår i: Inflammation Research. - : Springer Science and Business Media LLC. - 1420-908X .- 1023-3830. ; 56:5, s. 189-194
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To define the importance of leukocyte recruitment in endotoxin-induced gut permeability. Materials and methods: 31 male C57BL/6 mice were challenged with lipopolysaccharide (LPS). Ileal permeability was measured in Ussing chambers and leukocyte-endothelium interactions studied with intravital fluorescence microscopy after 18 h. Results: LPS caused a clear-cut increase in leukocyte accumulation and intestinal permeability. Immunoneutralisation of P-selectin not only reduced leukocyte recruitment significantly (54% reduction) but also abolished endotoxin-induced intestinal leakage. Intestinal levels of pro-inflammatory chemokines increased markedly in response to LPS but were not influenced by inhibition of P-selectin in vivo. Conclusion: The present study shows not only that endotoxin-induced leukocyte recruitment is mediated by P-selectin but also that sepsis-associated intestinal leakage in the gut is largely regulated by leukocyte accumulation. Thus, our novel data demonstrate a critical link between P-selectin-dependent leukocyte recruitment and gut barrier failure in endotoxemia.
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- Nilsson, Bengt-Olof
(författare)
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Modulation of the inflammatory response by estrogens with focus on the endothelium and its interactions with leukocytes.
- 2007
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Ingår i: Inflammation Research. - : Springer Science and Business Media LLC. - 1420-908X .- 1023-3830. ; 56:7, s. 269-273
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Forskningsöversikt (refereegranskat)abstract
- Gender differences and variations in inflammatory disease (e. g. atherosclerosis, neurological disorders, periodontitis and rheumatoid arthritis) severity with female sex hormone level have been reported, suggesting that female sex hormones modulate the inflammatory response. Estrogens act on gene transcription via estrogen receptors alpha and beta. Identification of estrogen-regulated genes is a matter of great interest since it will contribute significantly to the understanding of the physiological importance of estrogens. Anti-inflammatory as well as pro-inflammatory responses to estrogens have been reported. Data have been presented showing that estrogens down-regulate the expression of adhesion and chemokine molecules in response to inflammation promoters in various experimental systems. Functional data show that estrogen treatment attenuates recruitment and adhesion of leukocytes to the endothelium induced by inflammation promoters offering a possible mechanism by which estrogens exert an anti-inflammatory effect. These effects of estrogens, with focus on the interactions of monocytes with the vascular endothelium, are highlighted in this review.
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- Saiepour, Daniel, et al.
(författare)
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Insulin inhibits phagocytosis in normal human neutrophils via PKCalpha/beta-dependent priming of F-actin assembly.
- 2006
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Ingår i: Inflammation Research. - : Springer Science and Business Media LLC. - 1023-3830 .- 1420-908X. ; 55:3, s. 85-91
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: This study investigated the effects of insulin on the phagocytosis of C3bi - and IgG-opsonized yeast particles in normal human neutrophils. METHODS: Neutrophils were incubated in different insulin concentrations for 30 minutes and stimulated by C3bi - or IgG-opsonized yeast particles. Phagocytosis was quantified by both light microscopy and FACscan flow cytometry. Laser confocal microscopy was used for quantification of F-actin levels. RESULTS: Elevated insulin concentrations decreased neutrophil phagocytosis of both types of targets. This defect was shown to be in part due to a delayed phagocytosis in the presence of insulin. Following a 30 minute incubation, insulin was found to increase the accumulation of cortical F-actin, without affecting the total cellular F-actin content. The specific PKCalpha/beta inhibitor, Go6976, abolished the insulin-mediated increase in cortical F-actin content and both Go6976 and the PKCalpha/beta/delta/epsilon-specific inhibitor GF109203X reversed the inhibitory effects of insulin on phagocytosis. CONCLUSION: Hyperinsulinemia in vitro can inhibit phagocytosis of opsonized targets in normal human neutrophils. This effect of insulin is dependent on activation of PKCalpha and/or PKCbeta, and these insulin signals may interfere with the dynamic assembly/disassembly and/or distribution of F-actin, which is required for the phagocytosis process.
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