COF-based artificial probiotic for modulation of gut microbiota and immune microenvironment in inflammatory bowel disease - PubMed (original) (raw)

. 2022 Dec 27;14(6):1598-1605.

doi: 10.1039/d2sc04984h. eCollection 2023 Feb 8.

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COF-based artificial probiotic for modulation of gut microbiota and immune microenvironment in inflammatory bowel disease

Qingqing Deng et al. Chem Sci. 2022.

Abstract

Conventional strategies for treating inflammatory bowel disease merely relieve inflammation and excessive immune response, but fail to solve the underlying causes of IBD, such as disrupted gut microbiota and intestinal barrier. Recently, natural probiotics have shown tremendous potential for the treatment of IBD. However, probiotics are not recommended for IBD patients, as they may cause bacteremia or sepsis. Herein, for the first time, we constructed artificial probiotics (Aprobiotics) based on artificial enzyme-dispersed covalent organic frameworks (COFs) as the "organelle" and a yeast shell as the membrane of the Aprobiotics to manage IBD. The COF-based artificial probiotics, with the function of natural probiotics, could markedly relieve IBD by modulating the gut microbiota, suppressing intestinal inflammation, protecting the intestinal epithelial cells, and regulating immunity. This nature-inspired approach may aid in the design of more artificial systems for the treatment of various incurable diseases, such as multidrug-resistant bacterial infection, cancer, and others.

This journal is © The Royal Society of Chemistry.

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Conflict of interest statement

All authors declare no competing interests.

Figures

Fig. 1

Fig. 1. Schematic illustration of the design of COF-based artificial probiotics for IBD therapy. (a) The synthesis of artificial probiotics. (b) The artificial probiotics for the treatment of IBD by modulating the gut microbiota, suppressing intestinal inflammation, protecting the intestinal epithelial cells, and regulating immunity .

Fig. 2

Fig. 2. Characterization of COF-based artificial probiotics and other related materials. (a) TEM image and (b) XRD pattern of the Aprobiotics. (c) Zeta-potential of the prepared COF, COF@Au, yeast, YS, YS-PEI and Aprobiotics. (d) XPS peak of COF, COF@Au and the Aprobiotics.

Fig. 3

Fig. 3. The artificial probiotic exerted bioactivities in vitro (a and b) Measurement of gluconic acid product after Aprobiotics and glucose were incubated in PBS (pH = 7.4). (c) The variation in pH value of the Aprobiotic solution in the absence and presence of glucose in 0.5 mM PBS (pH = 7.4). (d) O2 concentration change of Aprobiotic solution upon the addition of glucose in PBS (pH = 7.4). (e) O2˙− scavenging activity of Au, COF, COF@Au, YS and Aprobiotics. (f) O2˙− scavenging activity of different concentrations of Aprobiotics. (g) OH˙ scavenging activity of Aprobiotics. (h) ABTS+˙ scavenging activity of COF, COF@Au, YS and Aprobiotics. (i) ABTS+˙ scavenging activity of different concentrations of Aprobiotics.

Fig. 4

Fig. 4. Artificial probiotics suppressed excessive inflammatory response and reprogrammed the macrophage. (a) Fluorescence images and (b) flow cytometry analysis of ROS generation in RAW 264.7 cells treated with either H2O2 or Aprobiotics. (c) Immunofluorescent staining assay of macrophages after treatment with Aprobiotics for 1 day. (d) qPCR results of IL-10, TNF-α, Arg-1 and iNOS, respectively.

Fig. 5

Fig. 5. Artificial probiotics exert outstanding efficacy in DSS-induced ulcerative colitis (UC) models: (a) the change in colon length of each group, (b) relative body weight change throughout the experiment, (c) H&E-staining assay of mice colon on day 12.

Fig. 6

Fig. 6. Artificial probiotics modulated the gut microbiota and immune microenvironment. (a) Assessment of bacterial community richness (OUT). (b) PcoA analysis of the gut microbiome (c) Venn diagram of detected bacterial strains. (d) Relative abundance of the intestinal microbiome. (e) Heatmap of the relative abundance of bacterial taxa for each sample. (f) Circular plot representation of the interaction between genera of the gut microbial community of IBD mice after treatment with COF, COF@Au, and Aprobiotics. (g) Histological studies with immunohistochemical staining of mice colon on day 12.

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