Amelioration of DSS-Induced Acute Colitis in Mice by Recombinant Monomeric Human Interleukin-22

Kim, Suhyun; Hong, Eock Kee; Lee, Cheol-Ki; Ryu, Yiseul; Jeong, Hyunjin; Heo, Seungnyeong; Lee, Joong-Jae; Ko, Hyun‐Jeong

doi:10.4110/in.2022.22.e26

Cited by 6 publications

(3 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…38 In contrast to IL-10, the specifically expressed IL-22 in the intestine stimulated the regeneration of epithelial cells and increased the expression of antibacterial proteins, mucins, and tight junction proteins to protect its epithelial barrier. 39 Recently, monomeric IL-22 treatment was reported to inhibit the production of pro-inflammatory cytokines and alleviate DSS-induced acute colitis in mice, 40 and increased serum content and enhanced colonic expression of IL-22 were widely found to be associated with improved colitis phenotypes. 3 Our results revealed that UroA treatment significantly increased serum IL-22 levels, as expected, and decreased the content of IL-10 in serum (Figures 3C and 6F), suggesting that the anticolitis activity of UroA was primarily related to IL-22 in this study.…”

Section: Discussionmentioning

confidence: 99%

Urolithin A Alleviates Colitis in Mice by Improving Gut Microbiota Dysbiosis, Modulating Microbial Tryptophan Metabolism, and Triggering AhR Activation

Wang

Fan

et al. 2023

J. Agric. Food Chem.

View full text Add to dashboard Cite

Urolithin A (UroA) is a microbial metabolite derived from ellagitannins and ellagic acid with good bioavailability. In this study, we explored the anticolitis activity of UroA and clarified the mechanism by 16S rDNA sequencing and metabonomics. UroA alleviated dextran sulfate sodium (DSS)-induced colitis in mice, characterized by a decreased disease activity index, increased colon length, and improved colonic histopathological lesions, along with inhibited phosphorylation of the mitogen-activated protein kinase signaling pathway. In addition, UroA improved gut microbiota dysbiosis and modulated the microbiota metabolome. Furthermore, targeted metabolomics focused on tryptophan catabolites showed that UroA significantly increased the production of indole-3-aldehyde (IAld) and subsequently led to increased colonic expression of aryl hydrocarbon receptor (AhR) and promoted the serum content of IL-22 in mice with colitis. Collectively, our data identified a novel anticolitis mechanism of UroA by improving gut microbiota dysbiosis, modulating microbial tryptophan metabolism, promoting IAld production, and triggering AhR/IL-22 axis activation. However, a limitation noted in this study is that these beneficial effects of UroA were found at 50 μM in vitro and 20 mg/ kg in vivo, which were nonphysiological concentrations.

show abstract

Section: Discussionmentioning

confidence: 99%

Urolithin A Alleviates Colitis in Mice by Improving Gut Microbiota Dysbiosis, Modulating Microbial Tryptophan Metabolism, and Triggering AhR Activation

Wang

Fan

et al. 2023

J. Agric. Food Chem.

View full text Add to dashboard Cite

show abstract

“…4c). Treatment with recombinant IL-22 ameliorated DSSinduced colitis in WT mice 46 but not in ERdj5-KO mice (Supplementary Fig. 3d).…”

Section: Erdj5 Helps Maintain Gut Barrier Function By Enhancing Tight...mentioning

confidence: 94%

ERdj5 protects goblet cells from endoplasmic reticulum stress-mediated apoptosis under inflammatory conditions

et al. 2023

Self Cite

View full text Add to dashboard Cite

Endoplasmic reticulum stress is closely associated with the onset and progression of inflammatory bowel disease. ERdj5 is an endoplasmic reticulum-resident protein disulfide reductase that mediates the cleavage and degradation of misfolded proteins. Although ERdj5 expression is significantly higher in the colonic tissues of patients with inflammatory bowel disease than in healthy controls, its role in inflammatory bowel disease has not yet been reported. In the current study, we used ERdj5-knockout mice to investigate the potential roles of ERdj5 in inflammatory bowel disease. ERdj5 deficiency causes severe inflammation in mouse colitis models and weakens gut barrier function by increasing NF-κB-mediated inflammation. ERdj5 may not be indispensable for goblet cell function under steady-state conditions, but its deficiency induces goblet cell apoptosis under inflammatory conditions. Treatment of ERdj5-knockout mice with the chemical chaperone ursodeoxycholic acid ameliorated severe colitis by reducing endoplasmic reticulum stress. These findings highlight the important role of ERdj5 in preserving goblet cell viability and function by resolving endoplasmic reticulum stress.

show abstract

“…The proteins were purified using Ni-NTA agarose affinity chromatography, following the standard protocol. [21] Size-exclusion chromatography using HiLoad® 16/600 Superdex® 75 column (Cytiva, USA) was performed to increase the purity of the proteins. The production and purification of the proteins were examined by SDS-PAGE and the concentration of the purified proteins was determined by Bradford assay.…”

Section: Protein Expression and Purificationmentioning

confidence: 99%

Protein Ligation‐Assisted Reconstitution of Split HRP Fragments for Facile Production of HRP Fusion Proteins in E. coli

et al. 2023

Self Cite

View full text Add to dashboard Cite

Horseradish peroxidase (HRP) is a pivotal biocatalyst for biosensor development and fine chemical synthesis. HRP proteins are mostly extracted and purified from the roots of horseradish because the solubility and productivity of recombinant HRP in bacteria are significantly low. In this study, we investigate the reconstitution system of split HRP fragments to improve its soluble expression levels in E. coli allowing the cost‐effective production of bioactive HRPs. To promote the effective association between two HRP fragments (HRPn and HRPc), we exploit SpyTag‐SpyCatcher chemistry, a versatile protein coupling method with high affinity and selectivity. Each HRP fragment was genetically fused with SpyTag and SpyCatcher, respectively, exhibiting soluble expression in the E. coli cytoplasm. The engineered split HRPs were effectively and irreversibly reconstituted into a biologically active and stable assembly that can catalyze intrinsic enzymatic reactions. Compared to the chaperone co‐expression system, our approach shows that the production yield of soluble HRP is comparable, but the purity of the final product is relatively high. Therefore, our results can be applied to the high‐yield production of recombinant HRP variants and other difficult‐to‐express proteins in bacteria without complex downstream processes.

show abstract

Amelioration of DSS-Induced Acute Colitis in Mice by Recombinant Monomeric Human Interleukin-22

Cited by 6 publications

References 61 publications

Urolithin A Alleviates Colitis in Mice by Improving Gut Microbiota Dysbiosis, Modulating Microbial Tryptophan Metabolism, and Triggering AhR Activation

Urolithin A Alleviates Colitis in Mice by Improving Gut Microbiota Dysbiosis, Modulating Microbial Tryptophan Metabolism, and Triggering AhR Activation

ERdj5 protects goblet cells from endoplasmic reticulum stress-mediated apoptosis under inflammatory conditions

Protein Ligation‐Assisted Reconstitution of Split HRP Fragments for Facile Production of HRP Fusion Proteins in E. coli

Contact Info

Product

Resources

About