Kim K C, Nassiri J, Brody J S
Pulmonary Center, Boston University School of Medicine, MA 02118.
Am J Respir Cell Mol Biol. 1989 Aug;1(2):137-43. doi: 10.1165/ajrcmb/1.2.137.
Confluent hamster tracheal surface epithelial (HTSE) cells in primary culture are enriched with secretory cells that synthesize and release mucins. Using this cell culture system, we investigated possible mechanisms of goblet cell mucin release by altering the media bathing the apical surface of HTSE cells: medium hyperosmolarity decreased mucin release, whereas hypo-osmolarity increased release without causing a cytoplasmic leak due to plasma membrane damage. A Ca2+ ionophore, A23187, did not influence mucin release. Both acidic (pH less than 4) and basic (pH greater than 9) media caused significant increases in mucin release secondary to cell membrane damage. Physiologic concentrations of chemical mediators such as prostaglandins (PGE2 and PGF2 alpha) and leukotrienes (LTC4 and LTD4) did not influence mucin release. Both elastase and cathepsin G derived from human neutrophils caused marked increases in release, whereas trypsin from the porcine pancreas produced a small increase only at a high concentration. We conclude that mucin release by cultured airway goblet cells can be enhanced by: (1) irritant gases, (2) luminal fluid osmolarity, (3) pharmacologic concentrations of LTC4 and LTD4, and (4) cationic proteases, each presumably acting by different mechanisms. Each of these mechanisms may play a role in epithelial mucin secretion associated with airway inflammation.
原代培养的融合仓鼠气管表面上皮（HTSE）细胞富含合成并释放粘蛋白的分泌细胞。利用该细胞培养系统，我们通过改变HTSE细胞顶端表面的培养液来研究杯状细胞粘蛋白释放的可能机制：培养液高渗降低粘蛋白释放，而低渗增加释放，且不会因质膜损伤导致细胞质泄漏。钙离子载体A23187不影响粘蛋白释放。酸性（pH小于4）和碱性（pH大于9）培养液均因细胞膜损伤导致粘蛋白释放显著增加。前列腺素（PGE2和PGF2α）和白三烯（LTC4和LTD4）等化学介质的生理浓度不影响粘蛋白释放。源自人中性粒细胞的弹性蛋白酶和组织蛋白酶G均导致释放显著增加，而来自猪胰腺的胰蛋白酶仅在高浓度时产生小幅增加。我们得出结论，培养的气道杯状细胞的粘蛋白释放可通过以下方式增强：（1）刺激性气体，（2）管腔液渗透压，（3）药理浓度的LTC4和LTD4，以及（4）阳离子蛋白酶，每种可能通过不同机制起作用。这些机制中的每一种都可能在与气道炎症相关的上皮粘蛋白分泌中起作用。
