INTERLEUKIN-8 IS A MAJOR NEUTROPHIL CHEMOTACTIC FACTOR IN PLEURAL LIQUID OF PATIENTS WITH EMPYEMA

INTERLEUKIN-8 IS A MAJOR NEUTROPHIL CHEMOTACTIC FACTOR IN PLEURAL LIQUID OF PATIENTS WITH EMPYEMA
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DOI:
10.1164/ajrccm/146.4.825
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发表时间:
1992-10-01
期刊:
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子:
--
通讯作者:
BOYLAN, AM
BOYLAN, AM
中科院分区:
其他
文献类型:
--
作者:
BROADDUS, VC;HEBERT, CA;BOYLAN, AM

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白细胞介素-8(IL-8)是一种有效的中性粒细胞趋化肽,已被发现与人类疾病有关,但其对人类趋化活性的贡献尚不清楚。我们询问IL-8是否存在于炎症性人胸腔积液中,以及它在多大程度上有助于胸腔液体中性粒细胞趋化活性。由于肿瘤坏死因子α (tnf - α)是IL-8的强诱导剂,我们也询问了tnf - α是否存在。在这项前瞻性研究中,我们收集了51例患者的胸膜液(脓胸14例,肺旁肺4例,结核8例,恶性9例,杂性渗出7例,渗出性9例),计算了胸膜中性粒细胞,并测量了上清液中IL-8和tnf - α的浓度。为了确定IL-8对脓腔趋化活性的贡献,我们测量了在加入抗IL-8 F(ab’)2抗体片段或对照抗il -6 F(ab’)2抗体片段前后脓腔液诱导的中性粒细胞迁移。我们发现,积液中IL-8浓度(61.3 +/- 21.0 ng/ml [SEM])高于其他所有积液(1.1 +/- 0.5 ng/ml) (p = 0.0001)。所有脓液的IL-8浓度均高于2.5 ng/ml,而其他37例积液中只有3例(2例肺旁积液,1例结核积液)的IL-8浓度高于2.5 ng/ml。IL-8水平与胸膜中性粒细胞计数(r = 0.46; p = 0.007)和胸膜液中性粒细胞趋化活性相关(r = 0.43; p = 0.008)。抗il -8抗体使脓胸液的趋化活性降低65 +/- 5%,而对照抗体无影响(降低0 +/- 5%)(p = 0.0005)。虽然抗原TNF- α在脓毒症(79%)和结核性(88%)积液中最常见,但TNF生物活性仅在脓毒症(9例积液中的4例)中检测到,而在结核性积液中未检测到(7例中0例)(p = 0.044)。我们得出结论,IL-8是胸气肿患者胸膜液中主要的中性粒细胞趋化因子,胸膜内tnf - α可能参与诱导IL-8的产生。
Interleukin-8(IL-8),a potent neutrophil chemotactic peptide, has been found in association with human disease, but its contribution to chemotactic activity In humans is not yet known. We asked whether IL-8 is present in inflammatory human pleural effusions, and to what extent it contributes to pleural liquid neutrophil chemotactic activity. Because tumor necrosis factor alpha (TNF-alpha) is a strong inducer of IL-8, we also asked whether TNF-alpha was present. For this prospective study, we collected pleural liquid from 51 patients (empyema, 14; parapneumonic, four; tuberculous, eight; malignant, nine; miscellaneous exudative, seven; and transudative, nine), counted pleural neutrophils, and measured IL-8 and TNF-alpha concentrations in the supernatant. To determine the contribution of IL-8 to chemotactic activity in empyema, we measured the neutrophil migration induced by empyemic liquids before and after addition of anti-IL-8 F(ab')2 antibody fragments or control anti-IL-6 F(ab')2. We found that IL-8 concentrations were higher in empyema (61.3 +/- 21.0 ng/ml [SEM]) than in all other effusions (1.1 +/- 0.5 ng/ml) (p = 0.0001). All empyema liquids had IL-8 concentrations above 2.5 ng/ml, which was true for only three of the other 37 effusions (two parapneumonic, one tuberculous). IL-8 levels correlated with the pleural neutrophil count (r = 0.46; p = 0.007) and the neutrophil chemotactic activity of pleural liquid (r = 0.43; p = 0.008). Anti-IL-8 antibodies decreased chemotactic activity in empyema liquids by 65 +/- 5%, whereas the control antibody had no effect (0 +/- 5% decrease) (p = 0.0005). Although antigenic TNF-alpha was found most frequently in empyemic (79% of effusions) and tuberculous (88%) effusions, TNF bioactivity was detected only in empyemic (four of nine effusions), not in tuberculous effusions (zero of seven) (p = 0.044). We conclude that IL-8 represents a major neutrophil chemotactic factor in the pleural liquid of patients with empyema and that intrapleural TNF-alpha may participate in induction of IL-8 production.