Department of Microbiology and Immunology, University of Texas Medical Branch, 301 University Boulevard, Galveston, Texas 77555, USA.
Infect Immun. 2010 Apr;78(4):1740-9. doi: 10.1128/IAI.01114-09. Epub 2010 Feb 1.
Enterotoxigenic Escherichia coli (ETEC) produces the ADP-ribosyltransferase toxin known as heat-labile enterotoxin (LT). In addition to the toxic effect of LT resulting in increases of cyclic AMP (cAMP) and disturbance of cellular metabolic processes, this toxin promotes bacterial adherence to intestinal epithelial cells (A. M. Johnson, R. S. Kaushik, D. H. Francis, J. M. Fleckenstein, and P. R. Hardwidge, J. Bacteriol. 191:178-186, 2009). Therefore, we hypothesized that the identification of a compound that inhibits the activity of the toxin would have a suppressive effect on the ETEC colonization capabilities. Using in vivo and in vitro approaches, we present evidence demonstrating that a fluorenone-based compound, DC5, which inhibits the accumulation of cAMP in intoxicated cultured cells, significantly decreases the colonization abilities of adenylyl cyclase toxin-producing bacteria, such as ETEC. These findings established that DC5 is a potent inhibitor both of toxin-induced cAMP accumulation and of ETEC adherence to epithelial cells. Thus, DC5 may be a promising compound for treatment of diarrhea caused by ETEC and other adenylyl cyclase toxin-producing bacteria.
肠产毒性大肠杆菌(ETEC)产生一种称为不耐热肠毒素(LT)的 ADP-核糖基转移酶毒素。除了 LT 的毒性作用导致环腺苷酸(cAMP)增加和细胞代谢过程紊乱外,这种毒素还促进细菌黏附于肠上皮细胞(A.M. Johnson、R.S. Kaushik、D.H. Francis、J.M. Fleckenstein 和 P.R. Hardwidge,J. Bacteriol. 191:178-186,2009)。因此,我们假设鉴定一种抑制毒素活性的化合物将对 ETEC 定植能力具有抑制作用。我们采用体内和体外方法,提供了证据证明,一种基于芴酮的化合物 DC5 可抑制毒素感染的培养细胞中 cAMP 的积累,显著降低产腺苷酸环化酶毒素的细菌(如 ETEC)的定植能力。这些发现表明,DC5 是一种有效的抑制剂,可同时抑制毒素诱导的 cAMP 积累和 ETEC 黏附于上皮细胞。因此,DC5 可能是治疗由 ETEC 和其他产腺苷酸环化酶毒素的细菌引起的腹泻的一种有前途的化合物。