Hastie A T, Everts K B, Cho S K, Zangrilli J, Shaver J R, Pollice M B, Fish J E, Peters S P
Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Cytokine. 1996 Sep;8(9):730-8. doi: 10.1006/cyto.1996.0097.
This work investigated whether interleukin 1 beta (IL-1 beta) release from epithelial cells is modulated by antigen challenge in vivo, and inflammatory cells in vitro. Bronchial epithelial cells were obtained before and after segmental allergen challenge in allergic and normal individuals, and were cultured with and without autologous bronchoalveolar lavage (BAL) cells. IL-1 beta in culture medium was quantitated by enzyme-linked immunoabsorbent assay (ELISA). Pre-challenge IL-1 beta levels from epithelial cells were similar in allergic (4.4 +/- 0.8 pg/ml, n = 32) and normal (6.8 +/- 1.7 pg/ml, n = 17) subjects. IL-1 beta levels were significantly elevated from epithelium with BAL cell co-culture vs without co-culture in both subject groups (allergic, 13.2 +/- 2.3 pg/ml, P = 0.006; normal: 16.4 +/- 4.0 pg/ml, P = 0.007). Post-challenge IL-1 beta from epithelial cells without BAL cells was increased in both groups, but significant only for allergic subjects (P = 0.003). Post-challenge IL-1 beta from epithelial with BAL cells changed little for allergic subjects (13.8 +/- 2.4 pg/ml), and increased for normal subjects (20.0 +/- 4.8 pg/ml). Decreased production of tumour necrosis factor alpha (TNF-alpha) was observed in allergic subjects (day 1: 447 pg/ml vs day 2: 258 pg/ml). Moreover, pre-challenge release of TNF-alpha and IL-1 beta levels from epithelial + BAL cells correlated well for allergic (r = 0.84) and normal subjects (r = 0.6), but post-challenge release correlated only in normal subjects (r = 0.90). These results indicate that bronchial epithelial cells and BAL cells interact, modulating release of these inflammatory cytokines.
本研究调查了体内抗原激发以及体外炎性细胞是否会调节上皮细胞释放白细胞介素1β(IL-1β)。在变应性个体和正常个体进行节段性变应原激发前后获取支气管上皮细胞,并在有和没有自体支气管肺泡灌洗(BAL)细胞的情况下进行培养。通过酶联免疫吸附测定(ELISA)对培养基中的IL-1β进行定量。变应性受试者(4.4±0.8 pg/ml,n = 32)和正常受试者(6.8±1.7 pg/ml,n = 17)激发前上皮细胞的IL-1β水平相似。在两个受试者组中,与无共培养相比,上皮细胞与BAL细胞共培养时IL-1β水平均显著升高(变应性组,13.2±2.3 pg/ml,P = 0.006;正常组:16.4±4.0 pg/ml,P = 0.007)。两组中无BAL细胞的上皮细胞激发后IL-1β均增加,但仅变应性受试者有统计学意义(P = 0.003)。变应性受试者有BAL细胞的上皮细胞激发后IL-1β变化不大(13.8±2.4 pg/ml),而正常受试者增加(20.0±4.8 pg/ml)。变应性受试者中观察到肿瘤坏死因子α(TNF-α)产生减少(第1天:447 pg/ml对第2天:258 pg/ml)。此外,变应性受试者(r = 0.84)和正常受试者(r = 0.6)激发前上皮+BAL细胞释放的TNF-α和IL-1β水平相关性良好,但激发后释放仅在正常受试者中具有相关性(r = 0.90)。这些结果表明支气管上皮细胞和BAL细胞相互作用,调节这些炎性细胞因子的释放。