Zychlinsky A, Fitting C, Cavaillon J M, Sansonetti P J
Unité de Pathogénie Microbienne Moléculaire, Institut National de la Santé et de la Recherche Médicale U389, Institut Pasteur, Paris, France.
J Clin Invest. 1994 Sep;94(3):1328-32. doi: 10.1172/JCI117452.
Peritoneal macrophages undergoing apoptosis induced by Shigella flexneri infection release the inflammatory cytokine interleukin 1 (IL-1), but not IL-6 or tumor necrosis factor alpha (TNF alpha). Wild type shigella causes a very fast and significant release of IL-1 from prestimulated peritoneal macrophages, before the cell's integrity is compromised. Both IL-1 alpha and IL-1 beta are released, IL-1 beta in its mature processed form. IL-1 is released from presynthesized cytoplasmic pools. These results demonstrate that bacteria-induced apoptosis of macrophages may play an active role in vivo by releasing IL-1, which in turn mediates an early inflammatory response in epithelial tissues.
受到福氏志贺菌感染诱导而发生凋亡的腹膜巨噬细胞会释放炎性细胞因子白细胞介素1(IL-1),但不会释放IL-6或肿瘤坏死因子α(TNFα)。野生型志贺菌会在细胞完整性受损之前,促使预先刺激的腹膜巨噬细胞非常快速且显著地释放IL-1。IL-1α和IL-1β都会被释放,其中IL-1β是以其成熟的加工形式被释放。IL-1是从预先合成的细胞质池中释放出来的。这些结果表明,细菌诱导的巨噬细胞凋亡可能通过释放IL-1在体内发挥积极作用,而IL-1反过来又介导上皮组织中的早期炎症反应。