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间质性肺疾病患者肺泡巨噬细胞PGE2产生与抑制活性之间的相关性。

Correlation between PGE2 production and suppressor activity of alveolar macrophages from patients with interstitial lung diseases.

作者信息

Fireman E, Ben Efraim S, Greif J, Alguetti A, Ayalon D, Topilsky M

机构信息

Institute of Pulmonary and Allergic Diseases, Ichilov Hospital, Tel-Aviv, Israel.

出版信息

Immunol Lett. 1988 Jun;18(2):159-65. doi: 10.1016/0165-2478(88)90058-2.

Abstract

The suppressive activity of alveolar macrophages (AM) obtained from bronchoalveolar lavage (BAL), on PHA stimulation of autologous peripheral blood lymphocytes (APL) was evaluated. The effect on lymphocyte stimulation was evaluated by coculturing the AM and APL cells at a ratio of 1:1. PGE2 released by AM during the culture period was measured by a radioimmune assay. The patients included in the study were 11 cases with interstitial lung disease (ILD), 8 cases of lung cancer (CA), and 5 controls (CO). Addition of AM of patients from the CA group resulted in slight suppression of lymphocyte stimulation in 4 cases, slight enhancement in 3 cases and no effect in one case. AM from the CO group induced slight suppression in 4 out of 5 cases. AM from all 11 ILD cases exerted a significant high suppressive activity (65.6% +/- 18.2 - P less than 0.001 by comparison with the CO and CA groups). In ILD cases, a dichotomous pattern was found in regard to relation between high suppressive activity of AM and release of PGE2: in idiopathic pulmonary fibrosis (IPF) patients, high suppressive activity of AM (70.4% +/- 15.4) correlated well with elevated secretion of PGE2: 3.58 +/- 0.26 ng/ml/10(5) cells (P less than 0.02 compared to CO). AM from sarcoidosis patients suppressed PHA stimulation by 61.6% +/- 19.3 but secreted only 0.357 +/- 0.26 ng/ml/10(5) cells of PGE2 (P less than 0.02 compared with the idiopathic pulmonary fibrosis group). Therefore, it seems that other factors, in addition to PGE2, might be involved in the suppressive activity of AM from interstitial lung diseases.

摘要

评估了从支气管肺泡灌洗(BAL)获得的肺泡巨噬细胞(AM)对自体外周血淋巴细胞(APL)PHA刺激的抑制活性。通过以1:1的比例共培养AM和APL细胞来评估对淋巴细胞刺激的影响。通过放射免疫测定法测量培养期间AM释放的PGE2。纳入研究的患者包括11例间质性肺疾病(ILD)、8例肺癌(CA)和5例对照(CO)。CA组患者的AM加入后,4例淋巴细胞刺激略有抑制,3例略有增强,1例无影响。CO组的AM在5例中有4例引起轻微抑制。所有11例ILD患者的AM均具有显著的高抑制活性(与CO组和CA组相比,65.6%±18.2 - P小于0.001)。在ILD病例中,发现AM的高抑制活性与PGE2释放之间存在二分模式:在特发性肺纤维化(IPF)患者中,AM的高抑制活性(70.4%±15.4)与PGE2分泌升高密切相关:3.58±0.26 ng/ml/10(5)细胞(与CO组相比P小于0.02)。结节病患者的AM抑制PHA刺激61.6%±19.3,但仅分泌0.357±0.26 ng/ml/10(5)细胞的PGE2(与特发性肺纤维化组相比P小于0.02)。因此,除PGE2外,似乎其他因素也可能参与间质性肺疾病中AM的抑制活性。

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