Department of Medicine, Division of Infectious Diseases, University at Buffalo, Buffalo, NY 14221, USA.
Toxins (Basel). 2021 Jun 23;13(7):437. doi: 10.3390/toxins13070437.
Several classes of non-antibiotic drugs, including psychoactive drugs, proton-pump inhibitors (PPIs), non-steroidal anti-inflammatory drugs (NSAIDs), and others, appear to have strong antimicrobial properties. We considered whether psychoactive drugs induce the SOS response in bacteria and, consequently, induce Shiga toxins in Shiga-toxigenic (STEC). We measured the induction of an SOS response using a reporter strain, as RecA is an early, reliable, and quantifiable marker for activation of the SOS stress response pathway. We also measured the production and release of Shiga toxin 2 (Stx2) from a classic O157:H7 strain, derived from a food-borne outbreak due to spinach. Some, but not all, serotonin selective reuptake inhibitors (SSRIs) and antipsychotic drugs induced an SOS response. The use of SSRIs is widespread and increasing; thus, the use of these antidepressants could account for some cases of hemolytic-uremic syndrome due to STEC and is not attributable to antibiotic administration. SSRIs could have detrimental effects on the normal intestinal microbiome in humans. In addition, as SSRIs are resistant to environmental breakdown, they could have effects on microbial communities, including aquatic ecosystems, long after they have left the human body.
几类非抗生素药物，包括精神活性药物、质子泵抑制剂 (PPIs)、非甾体抗炎药 (NSAIDs) 等，似乎具有很强的抗菌特性。我们研究了精神活性药物是否会在细菌中诱导 SOS 反应，从而诱导产志贺毒素的大肠杆菌 (STEC) 产生志贺毒素。我们使用报告菌株来衡量 SOS 反应的诱导情况，因为 RecA 是激活 SOS 应激反应途径的早期、可靠和可量化的标记物。我们还测量了经典 O157:H7 菌株（源自因菠菜引起的食源性爆发）产生和释放志贺毒素 2 (Stx2) 的情况。一些但不是所有的选择性 5-羟色胺再摄取抑制剂 (SSRIs) 和抗精神病药物都会诱导 SOS 反应。SSRIs 的使用非常广泛且呈上升趋势；因此，这些抗抑郁药的使用可能是某些 STEC 引起的溶血性尿毒综合征的原因，而不能归因于抗生素的使用。SSRIs 可能会对人类的正常肠道微生物群产生不利影响。此外，由于 SSRIs 能抵抗环境破坏，因此它们可能会对包括水生生态系统在内的微生物群落产生影响，即使它们已经离开人体。
