Abstract

RATIONALE: We examined the mechanisms used by eosinophils (EOS) to accumulate on IL-13- or TNF-alpha- stimulated human unbilical vein endothelial cells (HUVECs) under flow conditions.METHODS: HUVECs were treated for 1, 3, 6, 18 and 24 hours with IL-13 or TNF-alpha (1-100 ng/ml). Human EOS were infused at physiologic flow rates (0.5 dyn/cm2) for 10 min, and attached EOS were counted.RESULTS: Under these flow conditions, EOS accumulated efficiently on IL-13-stimulated (109 ± 18 eos/field) or TNF-alpha-stimulated (96 ± 27 eos/field) HUVECs in a concentration dependent manner. EOS accumulation on IL-13-activated HUVECs was first observed at 6 hours and reached a maximum at 18 hours. On the other hand, the levels of EOS accumulating on TNF-alpha-activated HUVECs was the same at all time points (1,3, 6, 18, 24 hours). Anti-alpha4 integrin mAb inhibited EOS accumulation on both IL-13 and TNF-alpha activated HUVECs.CONCLUSIONS: EOS accumulation on HUVECs under these flow conditions is differently regulated by IL-13 and TNF-alpha. RATIONALE: We examined the mechanisms used by eosinophils (EOS) to accumulate on IL-13- or TNF-alpha- stimulated human unbilical vein endothelial cells (HUVECs) under flow conditions. METHODS: HUVECs were treated for 1, 3, 6, 18 and 24 hours with IL-13 or TNF-alpha (1-100 ng/ml). Human EOS were infused at physiologic flow rates (0.5 dyn/cm2) for 10 min, and attached EOS were counted. RESULTS: Under these flow conditions, EOS accumulated efficiently on IL-13-stimulated (109 ± 18 eos/field) or TNF-alpha-stimulated (96 ± 27 eos/field) HUVECs in a concentration dependent manner. EOS accumulation on IL-13-activated HUVECs was first observed at 6 hours and reached a maximum at 18 hours. On the other hand, the levels of EOS accumulating on TNF-alpha-activated HUVECs was the same at all time points (1,3, 6, 18, 24 hours). Anti-alpha4 integrin mAb inhibited EOS accumulation on both IL-13 and TNF-alpha activated HUVECs. CONCLUSIONS: EOS accumulation on HUVECs under these flow conditions is differently regulated by IL-13 and TNF-alpha.

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