Elevated TNF-alpha production by peripheral blood monocytes of weight-losing COPD patients
Elevated TNF-alpha production by peripheral blood monocytes of weight-losing COPD patients
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DOI：
10.1164/ajrccm.153.2.8564110
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发表时间：
1996-02-01
影响因子：
24.7
通讯作者：
Rogers, RM
中科院分区：
文献类型：
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作者：
deGodoy, I;Donahoe, M;Rogers, RM
炎症细胞因子，肿瘤坏死因子- α (tnf - α)和白细胞介素-1- β (IL-1 β)，在正常人体外源性给药后与加速代谢和蛋白质周转有关。我们假设这些炎性细胞因子可能有助于慢性阻塞性肺疾病（COPD）患者的减肥过程。如果COPD患者报告在前一年体重减轻5%，则前瞻性地将其确定为“减重者”（WL; n = 10）；如果其体重波动小于或等于5%，则前瞻性地将其确定为“体重稳定者”（WS; n = 10）。选取年龄匹配的健康志愿者作为对照组（C; n = 13）。从外周血样本中分离单核细胞，培养并暴露于脂多糖（LPS）中。采用四层增强ELISA法测定单核细胞上清液中tnf - α和IL-1 β的浓度。在三个研究人群中，lps刺激的IL-1 β的产生没有显著差异。然而，与WS患者（6.9[1.5至16.6]）和C组患者（5.7[0至61.8]）相比，WL COPD患者中lps刺激的单核细胞tnf - α生成（平均[范围]ng/ml）（20.2[6.3至44.8]）明显更高。在没有持续减肥的情况下，这种差异在6个月的随访中没有保持。要确定tnf - α产生与体重减轻之间的因果关系，需要进一步了解这些患者的能量代谢与tnf - α产生之间的关系。
The inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1 beta), have been associated with accelerated metabolism and protein turnover following exogenous administration in normal humans. We hypothesized that these inflammatory cytokines might contribute to the weight-losing process in patients with chronic obstructive pulmonary disease (COPD). COPD patients were identified prospectively as ''weight losers'' (WL; n = 10) if they reported > 5% weight loss during the preceding year or as ''weight stable'' (WS; n = 10) if their body weight fluctuated less than or equal to 5%. Age-matched healthy volunteers were selected as the control group (C; n = 13). Monocytes were isolated from a peripheral blood sample, cultured, and exposed to lipopolysaccharide (LPS). The concentration of TNF-alpha and IL-1 beta in the monocyte supernatant was measured using a four layer enhanced ELISA. No significant difference in LPS-stimulated IL-1 beta production was found in the three study populations. However, LPS-stimulated TNF-alpha production (mean [range] ng/ml) by monocytes was significantly higher in the WL COPD patients (20.2 [6.3 to 44.8]), compared with WS patients (6.9 [1.5 to 16.6]), and C subjects (5.7 [0 to 61.8]). This difference was not maintained at 6 mo follow-up in the absence of ongoing weight loss. Definition of a causal relationship between TNF-alpha production and weight loss will require further understanding of the relationship between energy metabolism and TNF-alpha production in these patients.