Department of Infection Biology, London School of Hygiene and Tropical Medicine, Keppel Street, London, WC1E 7HT, UK.
Randall Centre for Cell and Molecular Biophysics, King's College London, London, WC2R 2LS, UK.
Sci Rep. 2023 Jun 11;13(1):9492. doi: 10.1038/s41598-023-32656-8.
Treatment of Clostridioides difficile infection (CDI) is expensive and complex, with a high proportion of patients suffering infection relapse (20-35%), and some having multiple relapses. A healthy, unperturbed gut microbiome provides colonisation resistance against CDI through competition for nutrients and space. However, antibiotic consumption can disturb the gut microbiota (dysbiosis) resulting in the loss of colonisation resistance allowing C. difficile to colonise and establish infection. A unique feature of C. difficile is the production of high concentrations of the antimicrobial compound para-cresol, which provides the bacterium with a competitive advantage over other bacteria found in the gut. p-cresol is produced by the conversion of para-Hydroxyphenylacetic acid (p-HPA) by the HpdBCA enzyme complex. In this study, we have identified several promising inhibitors of HpdBCA decarboxylase, which reduce p-cresol production and render C. difficile less able to compete with a gut dwelling Escherichia coli strain. We demonstrate that the lead compound, 4-Hydroxyphenylacetonitrile, reduced p-cresol production by 99.0 ± 0.4%, whereas 4-Hydroxyphenylacetamide, a previously identified inhibitor of HpdBCA decarboxylase, only reduced p-cresol production by 54.9 ± 13.5%. To interpret efficacy of these first-generation inhibitors, we undertook molecular docking studies that predict the binding mode for these compounds. Notably, the predicted binding energy correlated well with the experimentally determined level of inhibition, providing a molecular basis for the differences in efficacy between the compounds. This study has identified promising p-cresol production inhibitors whose development could lead to beneficial therapeutics that help to restore colonisation resistance and therefore reduce the likelihood of CDI relapse.
艰难梭菌感染(CDI)的治疗既昂贵又复杂,很大一部分患者会遭受感染复发(20-35%),有些患者甚至会多次复发。健康、未受干扰的肠道微生物群通过竞争营养物质和空间为肠道提供定植抵抗能力,从而防止 CDI 定植和感染。然而,抗生素的使用会扰乱肠道微生物群(失调),导致定植抵抗能力丧失,使艰难梭菌定植并引发感染。艰难梭菌的一个独特特征是产生高浓度的抗菌化合物对羟苯乙酸(para-cresol),这使该细菌在肠道中其他细菌中具有竞争优势。p-cresol 是由 HpdBCA 酶复合物将对羟苯乙酸(p-HPA)转化而来。在这项研究中,我们已经确定了几种有希望的 HpdBCA 脱羧酶抑制剂,这些抑制剂可降低 p-cresol 的产生,使艰难梭菌更难与肠道定植的大肠杆菌菌株竞争。我们证明,先导化合物 4-羟基苯乙腈可将 p-cresol 的产生减少 99.0±0.4%,而之前被鉴定为 HpdBCA 脱羧酶抑制剂的 4-羟基苯乙酰胺仅将 p-cresol 的产生减少 54.9±13.5%。为了解释这些第一代抑制剂的疗效,我们进行了分子对接研究,预测了这些化合物的结合模式。值得注意的是,预测的结合能与实验确定的抑制水平很好地相关,为化合物之间疗效的差异提供了分子基础。这项研究确定了有希望的 p-cresol 产生抑制剂,其开发可能会带来有益的治疗方法,有助于恢复定植抵抗能力,从而降低 CDI 复发的可能性。