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首页> 外文期刊>Nutrition, metabolism, and cardiovascular diseases: NMCD >Influence of chylomicron remnants on human monocyte activation in vitro.
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Influence of chylomicron remnants on human monocyte activation in vitro.

机译：乳糜微粒残留对体外人单核细胞活化的影响。

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BACKGROUND AND AIMS: Atherosclerosis is known to be an inflammatory disease and there is increasing evidence that chylomicron remnants (CMR), the lipoproteins which carry dietary fats in the blood, cause macrophage foam cell formation and inflammation. In early atherosclerosis the frequency of activated monocytes in the peripheral circulation is increased, and clearance of CMR from blood may be delayed, however, whether CMR contribute directly to monocyte activation and subsequent egress into the arterial wall has not been established. Here, the contribution of CMR to activation of monocyte pro-inflammatory pathways was assessed using an in vitro model. METHODS AND RESULTS: Primary human monocytes and CMR-like particles (CRLP) were used to measure several endpoints of monocyte activation. Treatment with CRLP caused rapid and prolonged generation of reactive oxygen species by monocytes. The pro-inflammatory chemokines MCP-1 and IL-8 were secreted in nanogram quantities by the cells in the absence of CRLP. IL-8 secretion was transiently increased after CRLP treatment, and CRLP maintained secretion in the presence of pharmacological inhibitors of IL-8 production. In contrast, exposure to CRLP significantly reduced MCP-1 secretion. Chemotaxis towards MCP-1 was increased in monocytes pre-exposed to CRLP and was reversed by addition of exogenous MCP-1. CONCLUSION: Our findings indicate that CRLP activate human monocytes and augment their migration in vitro by reducing cellular MCP-1 expression. Our data support the current hypothesis that CMR contribute to the inflammatory milieu of the arterial wall in early atherosclerosis, and suggest that this may reflect direct interaction with circulating blood monocytes.
机译：背景与目的：动脉粥样硬化是一种炎症性疾病，越来越多的证据表明乳糜微粒残留物（CMR）是一种在血液中携带膳食脂肪的脂蛋白，可引起巨噬细胞泡沫细胞的形成和炎症。在早期的动脉粥样硬化中，外周循环中活化的单核细胞的频率增加，并且从血液中清除CMR可能会延迟，但是，尚未确定CMR是否直接促进单核细胞活化以及随后进入动脉壁。在这里，使用体外模型评估了CMR对单核细胞促炎途径激活的贡献。方法与结果：人类原代单核细胞和CMR样颗粒（CRLP）被用于测量单核细胞活化的几个终点。 CRLP的治疗导致单核细胞快速且长期产生活性氧。在不存在CRLP的情况下，细胞以纳克数量分泌促炎性趋化因子MCP-1和IL-8。在CRLP处理后，IL-8分泌会暂时增加，并且在存在IL-8产生的药理抑制剂的情况下，CRLP会维持分泌。相反，暴露于CRLP会显着降低MCP-1分泌。在预先暴露于CRLP的单核细胞中，对MCP-1的趋化性增加，并通过添加外源MCP-1逆转。结论：我们的发现表明CRLP通过减少细胞MCP-1表达来激活人单核细胞并增加其迁移。我们的数据支持当前的假设，即CMR有助于早期动脉粥样硬化的动脉壁炎性环境，并表明这可能反映了与循环血液单核细胞的直接相互作用。

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