Department of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC 29208, USA.
Department of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC 29208, USA.
Pharmacol Res. 2021 May;167:105548. doi: 10.1016/j.phrs.2021.105548. Epub 2021 Mar 15.
Acute Respiratory Distress Syndrome (ARDS) is triggered by a variety of agents, including Staphylococcal Enterotoxin B (SEB). Interestingly, a significant proportion of patients with COVID-19, also develop ARDS. In the absence of effective treatments, ARDS results in almost 40% mortality. Previous studies from our laboratory demonstrated that resveratrol (RES), a stilbenoid, with potent anti-inflammatory properties can attenuate SEB-induced ARDS. In the current study, we investigated the role of RES-induced alterations in the gut and lung microbiota in the regulation of ARDS. Our studies revealed that SEB administration induced inflammatory cytokines, ARDS, and 100% mortality in C3H/HeJ mice. Additionally, SEB caused a significant increase in pathogenic Proteobacteria phylum and Propionibacterium acnes species in the lungs. In contrast, RES treatment attenuated SEB-mediated ARDS and mortality in mice, and significantly increased probiotic Actinobacteria phylum, Tenericutes phylum, and Lactobacillus reuteri species in both the colon and lungs. Colonic Microbiota Transplantation (CMT) from SEB-injected mice that were treated with RES as well as the transfer of L. reuteri into recipient mice inhibited the production of SEB-mediated induction of pro-inflammatory cytokines such as IFN-γ and IL-17 but increased that of anti-inflammatory IL-10. Additionally, such CMT and L. reuteri recipient mice exposed to SEB, showed a decrease in lung-infiltrating mononuclear cells, cytotoxic CD8+ T cells, NKT cells, Th1 cells, and Th17 cells, but an increase in the population of regulatory T cells (Tregs) and Th3 cells, and increase in the survival of mice from SEB-mediated ARDS. Together, the current study demonstrates that ARDS induced by SEB triggers dysbiosis in the lungs and gut and that attenuation of ARDS by RES may be mediated, at least in part, by alterations in microbiota in the lungs and the gut, especially through the induction of beneficial bacteria such as L. reuteri.
急性呼吸窘迫综合征(ARDS)是由多种因素引起的,包括葡萄球菌肠毒素 B(SEB)。有趣的是,相当一部分 COVID-19 患者也会发展为 ARDS。在缺乏有效治疗方法的情况下,ARDS 的死亡率接近 40%。我们实验室的先前研究表明,白藜芦醇(RES),一种具有强大抗炎特性的芪类化合物,可以减轻 SEB 诱导的 ARDS。在目前的研究中,我们研究了 RES 诱导的肠道和肺部微生物组改变在调节 ARDS 中的作用。我们的研究表明,SEB 给药会诱导 C3H/HeJ 小鼠产生炎症细胞因子、ARDS 和 100%的死亡率。此外,SEB 会导致肺部致病性变形菌门和痤疮丙酸杆菌属的显著增加。相比之下,RES 治疗可减轻 SEB 介导的 ARDS 和小鼠死亡率,并显著增加结肠和肺部中的有益菌放线菌门、厚壁菌门和雷氏乳杆菌属。用 RES 处理 SEB 注射小鼠的结肠微生物群移植(CMT)以及将雷氏乳杆菌属转移到受体小鼠中,可抑制 SEB 介导的促炎细胞因子(如 IFN-γ 和 IL-17)的产生,但增加抗炎性细胞因子 IL-10 的产生。此外,暴露于 SEB 的这种 CMT 和雷氏乳杆菌属受体小鼠,肺部浸润的单核细胞、细胞毒性 CD8+T 细胞、NKT 细胞、Th1 细胞和 Th17 细胞减少,而调节性 T 细胞(Tregs)和 Th3 细胞增加,以及 SEB 介导的 ARDS 小鼠的存活率增加。总之,目前的研究表明,SEB 诱导的 ARDS 会引发肺部和肠道的微生物失调,而 RES 减轻 ARDS 可能至少部分是通过肺部和肠道微生物组的改变介导的,特别是通过诱导有益细菌,如雷氏乳杆菌属。