| Autor: |
Leuenroth, S., Lee, C., Grutkoski, P., Keeping, H., Simms, H. |
| Zdroj: |
Surgery; August 1998, Vol. 124 Issue: 2 p409-417, 9p |
| Abstrakt: |
Background: Neutrophil apoptosis is crucial in the resolution of inflammation. The role of interleukin (IL)-8 in neutrophil apoptosis has not been previously studied; we hypothesized that in addition to its role as a chemoattractant, IL-8 would regulate polymorphonuclear leukocyte (PMN) apoptosis. Methods: PMNs were adhered to plastic during hypoxia or normoxia and treated with IL-8 dosages of 0 to 1000 ng/mL. Apoptosis was assessed by cellular histology and the TUNEL assay. For receptor inhibition, blocking antibodies to IL-8 receptors in the presence of IL-8 were added. Apoptosis of PMNs treated with anti-Fas antibody +/- IL-8 was also analyzed. Results: After treatment with 100 ng/mL IL-8, apoptosis was decreased from an average of 39.1% to 9.3%. Inhibition of IL-8RA was able to restore apoptosis to 59.4%. Western analysis showed that with IL-8, there was a marginal decrease of total Fas protein, whereas Fas ligand was increased. After incubation with an apoptosis inducing-Fas antibody, average PMN apoptosis was 42.3%, whereas Fas antibody plus IL-8 reduced apoptosis to 9.5%. Conclusions: IL-8 not only promotes the inflammatory response by recruiting PMNs but also acts to suppress apoptosis mainly through the IL-8RA in an oxygen tension independent manner. The reduction in apoptosis is associated with changes in Fas and FasL where the presence of IL-8 suppresses the proapoptotic function of Fas-FasL interactions. (Surgery 1998;124:409-17.) |
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