Fireman E, Ben Efraim S, Greif J, Alguetti A, Ayalon D, Topilsky M
Department of Pulmonary and Allergic Diseases, Tel Aviv Medical Center, Israel.
Int J Immunopharmacol. 1989;11(7):751-60. doi: 10.1016/0192-0561(89)90129-x.
Two groups of patients suffering from interstitial lung diseases (ILD) namely sarcoidosis (SA) and idiopathic pulmonary fibrosis (IPF) were investigated for alveolar macrophages (AM), secretion of prostaglandin E2 (PGE2) and interleukin 1 (IL-1), together with superoxide anion (O2-) production. Peripheral blood monocytes (PBMO) of the same patients were examined concomitantly for suppressive activity. Consistent with previous results, AM obtained by bronchoalveolar lavage (BAL) from ILD patients markedly suppressed the effects of PHA stimulation of autologous peripheral blood lymphocytes (APL): 61.8 +/- 9.7% suppressive activity compared to 15.5 +/- 15.4% in the control group (CO) P less than 0.001. The AM suppressive activity was correlated with an increase in PGE2 secretion: 3.861 +/- 2.194 ng/10(5) cells/ml in the IPF group, but not in the sarcoid group: 0.217 +/- 0.116 ng/10(5) cells/ml (P less than 0.001 between them). On the other hand, IL-1 secretion by AM was greatly increased in sarcoid patients (308 +/- 196 U/ml) but was within the normal limits in IPF (27.3 +/- 28.8 U/ml, P less than 0.01 between them). Therefore, an inverse correlation was found between degree of PGE2 secretion and IL-1 release by AM in ILD. O2-production by AM was markedly increased in all ILD patients but this mechanism is apparently not involved in suppressive activity. PBMO originating from ILD patients were less suppressive than the corresponding AM.
对两组间质性肺疾病（ILD）患者，即结节病（SA）患者和特发性肺纤维化（IPF）患者，进行了肺泡巨噬细胞（AM）、前列腺素E2（PGE2）和白细胞介素1（IL-1）分泌以及超氧阴离子（O2-）产生情况的研究。同时对相同患者的外周血单核细胞（PBMO）的抑制活性进行了检测。与之前的结果一致，通过支气管肺泡灌洗（BAL）从ILD患者获得的AM显著抑制了PHA刺激自体外周血淋巴细胞（APL）的效应：抑制活性为61.8±9.7%，而对照组（CO）为15.5±15.4%，P<0.001。AM的抑制活性与PGE2分泌增加相关：IPF组为3.861±2.194 ng/10(5)细胞/ml，而结节病组则不然：0.217±0.116 ng/10(5)细胞/ml（两组间P<0.001）。另一方面，结节病患者AM分泌的IL-1大幅增加（308±196 U/ml），而IPF患者的IL-1分泌在正常范围内（27.3±28.8 U/ml，两组间P<0.01）。因此，在ILD中发现AM分泌的PGE2程度与IL-1释放之间呈负相关。所有ILD患者AM的O2-产生均显著增加，但该机制显然与抑制活性无关。源自ILD患者的PBMO的抑制作用比相应的AM弱。
