Martín Giménez Virna Margarita, Modrego Javier, Gómez-Garre Dulcenombre, Manucha Walter, de Las Heras Natalia
Instituto de Investigaciones en Ciencias Químicas, Facultad de Ciencias Químicas y Tecnológicas, Universidad Católica de Cuyo, San Juan 5400, Argentina.
Laboratorio de Riesgo Cardiovascular y Microbiota, Hospital Clínico San Carlos-Instituto de Investigación Sanitaria San Carlos (IdISSC), 28040 Madrid, Spain.
Int J Mol Sci. 2023 Jul 31;24(15):12249. doi: 10.3390/ijms241512249.
Inflammation and oxidative stress are critical underlying mechanisms associated with COVID-19 that contribute to the complications and clinical deterioration of patients. Additionally, COVID-19 has the potential to alter the composition of patients' gut microbiota, characterized by a decreased abundance of bacteria with probiotic effects. Interestingly, certain strains of these bacteria produce metabolites that can target the S protein of other coronaviruses, thereby preventing their transmission and harmful effects. At the same time, the presence of gut dysbiosis can exacerbate inflammation and oxidative stress, creating a vicious cycle that perpetuates the disease. Furthermore, it is widely recognized that the gut microbiota can metabolize various foods and drugs, producing by-products that may have either beneficial or detrimental effects. In this regard, a decrease in short-chain fatty acid (SCFA), such as acetate, propionate, and butyrate, can influence the overall inflammatory and oxidative state, affecting the prevention, treatment, or worsening of COVID-19. This review aims to explore the current evidence regarding gut dysbiosis in patients with COVID-19, its association with inflammation and oxidative stress, the molecular mechanisms involved, and the potential of gut microbiota modulation in preventing and treating SARS-CoV-2 infection. Given that gut microbiota has demonstrated high adaptability, exploring ways and strategies to maintain good intestinal health, as well as an appropriate diversity and composition of the gut microbiome, becomes crucial in the battle against COVID-19.
炎症和氧化应激是与新冠肺炎相关的关键潜在机制,它们会导致患者出现并发症和临床病情恶化。此外,新冠肺炎有可能改变患者肠道微生物群的组成,其特征是具有益生菌作用的细菌丰度降低。有趣的是,这些细菌的某些菌株会产生可作用于其他冠状病毒S蛋白的代谢产物,从而防止其传播及有害影响。同时,肠道生态失调的存在会加剧炎症和氧化应激,形成一个使疾病持续存在的恶性循环。此外,人们普遍认识到肠道微生物群可代谢各种食物和药物,产生可能具有有益或有害作用的副产物。在这方面,短链脂肪酸(如乙酸盐、丙酸盐和丁酸盐)的减少会影响整体炎症和氧化状态,进而影响新冠肺炎的预防、治疗或病情恶化。本综述旨在探讨有关新冠肺炎患者肠道生态失调的现有证据、其与炎症和氧化应激的关联、涉及的分子机制,以及肠道微生物群调节在预防和治疗SARS-CoV-2感染方面的潜力。鉴于肠道微生物群已显示出高度适应性,探索维持良好肠道健康以及肠道微生物组适当多样性和组成的方法和策略,在抗击新冠肺炎的战斗中变得至关重要。