Armstrong L, Millar A B
University of Bristol, Department of Hospital Medicine, Southmead Hospital, Westbury on Trym, UK.
Thorax. 1997 May;52(5):442-6. doi: 10.1136/thx.52.5.442.
The adult respiratory distress syndrome (ARDS) may be regarded as an example of an uncontrolled or excessive inflammatory response in which tumour necrosis factor alpha (TNF-alpha) has been proposed to play a central role. Interleukin 10 (IL-10) has been identified as an important regulator of this response. The potential role for IL-10 in this context was investigated by measuring the relative production of IL-10 and TNF-alpha protein in the plasma, bronchoalveolar lavage (BAL) fluid, and alveolar macrophage culture supernatants of patients with, or at risk of developing, ARDS.
Twenty six patients were studied from three groups at risk of or with ARDS: sepsis (n = 12), multiple trauma (n = 8), and perforated bowel (n = 6). Ten patients had ARDS. Bronchoalveolar lavage and venepuncture were performed within 24 hours of arrival on the intensive therapy unit or of diagnosis of ARDS. IL-10 and TNF-alpha protein were detected in the plasma, BAL fluid, and alveolar macrophage supernatants by sandwich enzyme linked immunoabsorbent assays.
The median IL-10 concentrations in the plasma and BAL fluid of patients with ARDS were significantly lower than the concentrations detectable in the plasma (median difference-17.5, 95% CI -52.4 to 1.31, p < 0.05) and BAL fluid of at risk patients (median difference -32.1, 95% CI -47.5 to 2.3, p < 0.05). There was a tendency towards enhanced concentrations of TNF-alpha detectable in the alveolar macrophage supernatants and the BAL fluid of patients with ARDS compared with at risk patients, although this did not reach statistical significance. No difference was observed in the plasma concentrations of TNF-alpha between the two groups. The ratios of TNF-alpha to IL-10 protein in the BAL fluid of patients with ARDS and at risk patients were 3.52 and 0.85, respectively (median difference 1.44, 95% CI 0.07 to 5.01, p < 0.01). There was no difference in alveolar macrophage production of IL-10 between the two groups.
This study highlights the potential importance of the pro-inflammatory versus the anti-inflammatory imbalance in ARDS which may be reflected by the ratio of IL-10 and TNF-alpha in the lung.
成人呼吸窘迫综合征（ARDS）可被视为一种失控或过度的炎症反应，其中肿瘤坏死因子α（TNF-α）被认为起核心作用。白细胞介素10（IL-10）已被确定为这种反应的重要调节因子。通过测量ARDS患者或有发生ARDS风险患者的血浆、支气管肺泡灌洗（BAL）液和肺泡巨噬细胞培养上清液中IL-10和TNF-α蛋白的相对产生量，研究了IL-10在这种情况下的潜在作用。
对三组有ARDS风险或患有ARDS的患者进行了研究：脓毒症（n = 12）、多发伤（n = 8）和肠穿孔（n = 6）。10例患者患有ARDS。在入住重症监护病房后24小时内或诊断为ARDS后进行支气管肺泡灌洗和静脉穿刺。通过夹心酶联免疫吸附测定法检测血浆、BAL液和肺泡巨噬细胞上清液中的IL-10和TNF-α蛋白。
ARDS患者血浆和BAL液中IL-10浓度中位数显著低于有风险患者血浆（中位数差异-17.5，95%可信区间-52.4至1.31，p < 0.05）和BAL液中可检测到的浓度（中位数差异-32.1, 95%可信区间-47.5至2.3，p < 0.05）。与有风险患者相比，ARDS患者肺泡巨噬细胞上清液和BAL液中可检测到的TNF-α浓度有升高趋势，尽管未达到统计学显著性。两组患者血浆中TNF-α浓度无差异。ARDS患者和有风险患者BAL液中TNF-α与IL-10蛋白的比值分别为3.52和0.85（中位数差异1.44，95%可信区间0.07至5.01，p < 0.01）。两组肺泡巨噬细胞产生IL-10无差异。
本研究强调了ARDS中促炎与抗炎失衡的潜在重要性，这可能通过肺中IL-10和TNF-α的比值反映出来。
