Effect of Eotaxin on the Generationof Reactive Oxygen Species from Eosinophil Cell Line, YY-1

Abstract

Background: The CC chemokine eotaxin is a selective chemoattractant for eosinophils. Eosinophils have been considered to be the major effector cells in allergic inflammation, since not only eosinophil-specific granule proteins but also reactive oxygen species (ROS) from eosinophils may cause the damage to the cells or tissue of the mucosal epithelium. In this study, we examined the effect of eotaxin on ROS from an eosinophil cell line, YY-1. Methods: ROS in luminol-dependent reaction were examined. Calcium ionophore A23187 were added to the mixture of YY-1 cells with luminol, and then ROS were determined. Results: Eotaxin primed the production of ROS from YY-1 cells. ROS from untreated YY-1 cells evoked with calcium ionophore A23187 in luminol-dependent chemiluminescence gave a maximal value of 1,928 ± 223 intensity counts (IC; mean ± SE, n = 4) and an integral value of 17.04 ± 1.51 IC (×10^–4), while eosinophils that were treated with eotaxin gave a maximal value of 2,264 ± 86 IC (10 nM), 2,691 ± 124 IC (100 nM) and an integral value of 21.22 ± 0.67 IC (×10^–4; 10 nM), 26.20 ± 1.41 IC (×10^–4; 100 nM). Conclusion: Eotaxin might play important roles in the pathogenesis of allergic inflammation through eosinophil activation by priming of eosinophil oxidative metabolism as well as involvement in selective eosinophil chemotaxis.

CCL11 enhances excitotoxic neuronal death by producing reactive oxygen species in microglia

“…Consistent with this, CCL11 promoted migration and ROS production in microglia, as reported previously in eosinophils (Honda et al, 1999). In addition, we showed that microglia predominantly express CCR3, the main receptor for CCL11.…”

“…Thus, our data suggest that microglia are the main effectors of CCL11 in the CNS. Consistent with this, CCL11 promoted migration and ROS production in microglia, as reported previously in eosinophils (Honda et al, 1999). Moreover, CCL11-mediated microglial ROS potentiated excitotoxic neuronal death, a causative mechanism of neurodegeneration in various neurological disorders.…”

Interleukin-18 enhances the production of interleukin-8 by eosinophils

“…In addition, it is difficult to obtain sufficient eosinophils for functional analysis due to their small numbers in the peripheral blood cells. We therefore checked expression of IL-18R in the human eosinophilic cell lines, YY-1 [21,22] and EoL-1 [23] and other human cell lines including B cells (NALM6, RAMOS, DND39), myeloma cells (U266), T cells (Jurkat), monocytic cells (U937) and basophilic cells (KU812). As shown in Fig…”

“…Since YY-1 cells are known to differentiate into more mature eosinophils following treatment with n-butyric acid (n-BA), as measured by the cellular contents of granules and cytokines [21,22], the effect of n-BA on the expression of § chain of IL-18R in YY-1 cells was studied by RT-PCR and FACS analyses. As shown in Fig.…”

“…These observations prompted us to examine the effects of IL-18 on eosinophils. The expression of IL-18 § chain receptor was monitored on peripheral blood eosinophils and two human eosinophilic cell lines, YY-1 [21,22] and EoL-1 [23]. Incubation of YY-1 cells with IL-18 enhanced IL-8 synthesis.…”