Vinsamlegast notið þetta auðkenni þegar þið vitnið til verksins eða tengið í það: http://hdl.handle.net/1946/20666
Resolution of inflammation is important in preventing chronic inflammation. Natural killer (NK) cells are known to act as the first line of defence during an infection. This study examined the role of NK cells in the resolution of antigen-induced inflammation. Mice were injected intravenously with the NK cell depleting antibody, anti-asialo GM1, or a control antibody. Prior to NK cells depletion, the mice were immunized twice subcutaneously with methylated BSA (mBSA) and 24 hours after depletion, peritonitis was induced by injecting mBSA into their peritoneum. Prior to and at several time-points following peritonitis induction, peritoneal exudates were collected, cells counted and expression of surface molecules determined by flow cytometry. Concentrations of cytokines, soluble cytokine receptors and growth factors were determined by ELISA. The NK cell depletion antibody decreased the number of NK cells in the peritoneum by 50% 36 hours after injection of the antibody (12 h after induction of inflammation). Most of the NK cells were mature, CD11b+CD27+ cells. Immature CD11b-CD27+ NK cells increased after induction of inflammation in the control group but not in the depleted group. The NK cell depletion did not affect the expression of NK cell receptors. In the control group, neutrophils increased in numbers at 6 h and reached basal levels 48 h after induction of inflammation, whereas in the depleted group the neutrophils peaked at 12 h, and were at that time-point three time higher in number than that in the control group. In addition, in the depleted group the neutrophil numbers remained high throughout the study. NK cell depletion had little effect on the number or receptor expression of other cell types. The NK cell depletion increased the concentrations and /or prolonged higher levels of IL-6, IL-12p40, G-CSF and IL-1ra. These results demonstrate that NK cells affect the inflammation process and are necessary for resolution of antigen-induced inflammation.
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