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- Björkander, Sophia, et al.
(författare)
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Staphylococcus aureus-derived factors induce IL-10, IFN-gamma and IL-17A-expressing FOXP3(+)CD161(+) T-helper cells in a partly monocyte-dependent manner
- 2016
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Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 6
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Tidskriftsartikel (refereegranskat)abstract
- Staphylococcus aureus (S. aureus) is a human pathogen as well as a frequent colonizer of skin and mucosa. This bacterium potently activates conventional T-cells through superantigens and it is suggested to induce T-cell cytokine-production as well as to promote a regulatory phenotype in T-cells in order to avoid clearance. This study aimed to investigate how S. aureus impacts the production of regulatory and pro-inflammatory cytokines and the expression of CD161 and HELIOS by peripheral CD4(+)FOXP3(+) T-cells. Stimulation of PBMC with S. aureus 161:2-cell free supernatant (CFS) induced expression of IL-10, IFN-gamma and IL-17A in FOXP3(+) cells. Further, CD161 and HELIOS separated the FOXP3(+) cells into four distinct populations regarding cytokine-expression. Monocyte-depletion decreased S. aureus 161:2-induced activation of FOXP3(+) cells while pre-stimulation of purified monocytes with S. aureus 161:2-CFS and subsequent co-culture with autologous monocyte-depleted PBMC was sufficient to mediate activation of FOXP3(+) cells. Together, these data show that S. aureus potently induces FOXP3(+) cells and promotes a diverse phenotype with expression of regulatory and pro-inflammatory cytokines connected to increased CD161-expression. This could indicate potent regulation or a contribution of FOXP3(+) cells to inflammation and repression of immune-suppression upon encounter with S. aureus.
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| 7. |
- Rydén, Louise, 1975, et al.
(författare)
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Early inflammatory response in soft tissues induced by thin calcium phosphates.
- 2013
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Ingår i: Journal of biomedical materials research. Part A. - : Wiley. - 1552-4965 .- 1549-3296. ; 101A:9
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Tidskriftsartikel (refereegranskat)abstract
- The inflammatory response to titanium and hydroxyapatite (HA)-coated titanium in living tissue is controlled by a number of humoral factors, of which monocyte chemoattractant protein-1 (MCP-1) has been specifically linked to the recruitment of monocytes. These cells subsequently mature into tissue-bound macrophages. Macrophages adhering to the proteins adsorbed at the implant surface play a pivotal role in initiating the rejection or integration of the foreign material. Despite this, little is known about the initial inflammatory events that occur in soft tissues following the implantation of titanium and HA-coated titanium implants. In this study, circular discs of commercially pure titanium (c.p. Ti) with either a thin crystalline HA coating or amorphous HA coating or uncoated were implanted subcutaneously into rats. The implants were retrieved after 24 and 72 h. The lactate dehydrogenase (LD) activity, DNA content, expression of MCP-1, interleukin-10 (IL-10), tumor necrosis factor α (TNF-α), as well as monocyte and polymorphonuclear granulocyte counts in the exudate surrounding the implants were analyzed. There were significantly higher DNA and LD levels around the titanium implants at 24 h compared with HA-coated titanium. A rapid decrease in MCP-1 levels was observed for all the implants over the period of observation. No statistically significant differences were found between the two HA-coated implants. Our results suggest a difference in the early soft-tissue response to HA-coated implants when compared with titanium implants, expressed as a downregulation of inflammatory cell recruitment. This suggests that thin HA coatings are promising surfaces for soft tissue applications.
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| 8. |
- Thomsen, Peter, 1953, et al.
(författare)
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Preclinical in vivo models to study the inflammatory response to implants.
- 2006
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Ingår i: Abstract, Invited lecture, CIMTEC, Italy.
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Konferensbidrag (refereegranskat)abstract
- The interactions between the material surface and cellular and molecular components in the interface tissue are key features in the selection of optimal materials for clinical use. A quantitative analysis of the inflammatory, reparative and regenerative processes which occur as a response to implant modifications is therefore required. A prerequisite for such analyses is the development of experimental models which allow an access to sampling and harvesting of interfacial molecules, cells and tissues for subsequent analyses. The lecture will provide an overview of the features of such models and examples from own studies where biochemical, immunological and morphological techniques may be combined. We have developed a simple, reproducible experimental model in vivo, allowing a detailed analysis of initial inflammatory events as well as later, reparative processes in association with implant surfaces. Studies on the role of material bulk and surface properties for inflammatory cell chemotaxis, viability and cytokine patterns around materials will be discussed using metals, polymers, bioceramics and surface functionalizations.
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