Giménez-Scherer J A, Pacheco-Cano M G, Cruz de Lavín E, Hernández-Jáuregui P, Merchant M T, Kretschmer R R
Lab Invest. 1987 Jul;57(1):45-51.
The supernatant fluid of axenically grown Entamoeba histolytica-HM1 significantly modifies the ultrastructural features associated with monocyte chemotaxis as assayed in Boyden chambers. This morphological evidence supports the existence of a factor, monocyte locomotion inhibitory factor (MLIF), produced by E. histolytica that inhibits the in vitro locomotion of human monocytes. None of the leucocyte-locomotion modifying drugs included in this study (i.e., cytochalasin-B, colchicine, vinblastine, and hydrocortisone) caused changes totally comparable with those induced by MLIF. The most striking feature was the increase of centriole-associated microtubules induced by MLIF and by cytochalasin-B. MLIF may inhibit monocyte locomotion by directly inducing excessive microtubule assembly, although a direct, if somewhat weak effect upon microfilaments cannot be excluded. The increase in microtubules could then represent a perhaps futile attempt of the microtubule organizing center to overcome the locomotion blockade that has occurred elsewhere in the cell. If active in vivo, MLIF may contribute to the paucity of inflammation in the advanced stages of invasive amebiasis, and consequently to the lack of scar tissue formation upon recovery from such lesions, as monocytes constitute an essential link to the healing process.
在无共生菌培养的溶组织内阿米巴-HM1的上清液,可显著改变在Boyden小室中检测的与单核细胞趋化性相关的超微结构特征。这一形态学证据支持了溶组织内阿米巴产生一种单核细胞运动抑制因子(MLIF)的存在,该因子可抑制人单核细胞的体外运动。本研究中所包含的白细胞运动修饰药物(即细胞松弛素B、秋水仙碱、长春碱和氢化可的松)均未引起与MLIF诱导的变化完全可比的改变。最显著的特征是MLIF和细胞松弛素B诱导的中心粒相关微管的增加。MLIF可能通过直接诱导过度的微管组装来抑制单核细胞运动,尽管对微丝的直接作用(尽管有些微弱)也不能排除。微管的增加可能代表微管组织中心试图克服细胞其他部位发生的运动阻滞,但可能徒劳无功。如果MLIF在体内具有活性,它可能导致侵袭性阿米巴病晚期炎症的缺乏,从而导致从这些病变恢复后缺乏瘢痕组织形成,因为单核细胞是愈合过程的重要环节。