Intestinal vitamin D receptor knockout protects from oxazolone-induced colitis

Shi, Yongyan; Liu, Ziyun; Cui, Xuewei; Zhao, Qun; Liu, Tianjing

doi:10.1038/s41419-020-2653-3

Cited by 20 publications

(9 citation statements)

References 31 publications

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“…To date, the exact mechanism by which epithelial permeability changes has not been understood. Multiple inflammatory cytokines (such as TNF-a, IL-6, and IL-1β) secreted in the intestinal tract of UC patients may be the main cause of TJ destruction [17]. TJs play an important role in maintaining the integrity of the intestinal mucosal barrier, which is one of the strategies for the treatment of UC [18].…”

Section: Discussionmentioning

confidence: 99%

The Tryptophan Metabolite Indole-3-Carboxaldehyde Alleviates Mice with DSS-Induced Ulcerative Colitis by Balancing Amino Acid Metabolism, Inhibiting Intestinal Inflammation, and Improving Intestinal Barrier Function

et al. 2023

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Ulcerative colitis (UC) has attracted much attention for its negative influence on quality of life and increased risk of colorectal cancer. Chemical and biological drugs are currently the usual treatment for UC. These drugs always induce severe side effects, or patients might become resistant to these therapies. Therefore, new therapeutic options for UC are urgently needed. In this study, we discovered the inhibitory activity of the intestinal tryptophan metabolite indole-3-carboxaldehyde (3-IAld) in dextran sulfate sodium salt (DSS)-induced UC mice by targeting the TLR4/NF-κB/p38 signaling pathway. This compound effectively protected against colon length shortening and damage induced by DSS in the colon, notably reducing the severity of inflammation. The production of inflammatory factors of TNF-α, IL-6, and IL-1β was significantly attenuated when treating with 3-IAld in vivo and vitro. This might be attributed to inhibition of the TLR4/NF-kB/p38 signaling pathway. Moreover, 3-IAld could up-regulate the expression of ZO-1 and Occludin in vivo and vitro. Meanwhile, liquid chromatography mass spectrometry (LC-MS) results showed that 3-IAld could balance the aspartate and glutamate metabolism and the lysine degradation metabolism in the serum of DSS-induced colitis mice. In conclusion, 3-IAld ameliorated the intestinal barrier dysfunction and inflammatory response in DSS-induced UC mice, balanced amino acid metabolism, and inhibited the activation of the TLR4/NF-kB/p38 signaling pathway, thereby protecting mice with colitis.

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Section: Discussionmentioning

confidence: 99%

The Tryptophan Metabolite Indole-3-Carboxaldehyde Alleviates Mice with DSS-Induced Ulcerative Colitis by Balancing Amino Acid Metabolism, Inhibiting Intestinal Inflammation, and Improving Intestinal Barrier Function

et al. 2023

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“…DSS-induced colitis is broadly considered to be a ulcerative colitis–like model, and ulcerative colitis is considered a Th2-immune response (Gonzalez Acera et al 2021). However, the immune response in DSS-induced mice remains controversial (Chassaing et al 2014; Shi et al 2020), emphasizing the necessity to further understand the pathogenic roles of Th1 and Th2 responses in colitis.…”

Section: Discussionmentioning

confidence: 99%

Periodontitis Salivary Microbiota Worsens Colitis

et al. 2021

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Evidence suggests that periodontitis contributes to the pathogenesis of inflammatory bowel disease, including Crohn’s disease and ulcerative colitis. However, few studies have examined the role of swallowing and saliva in the pathogenesis of gastrointestinal diseases. Saliva contains an enormous number of oral bacteria and is swallowed directly into the intestine. Here, we explored the influence of periodontitis salivary microbiota on colonic inflammation and possible mechanisms in dextran sulfate sodium (DSS)–induced colitis. The salivary microbiota was collected from healthy individuals and those with periodontitis and gavaged to C57BL/6 mice. Periodontitis colitis was induced by DSS for 5 d and ligature for 1 wk. The degree of colon inflammation was evaluated through hematoxylin and eosin staining, ELISA, and quantitative real-time polymerase chain reaction. Immune parameters were measured with quantitative real-time polymerase chain reaction, flow cytometry, and immunofluorescence. The gut microbiota and metabolome analyses were performed via 16S rRNA gene sequencing and liquid chromatography–mass spectrometry. Although no significant colitis-associated phenotypic changes were found under physiologic conditions, periodontitis salivary microbiota exacerbated colitis in a periodontitis colitis model after DSS induction. The immune response more closely resembled the pathology of ulcerative colitis, including aggravated macrophage M2 polarization and Th2 cell induction (T helper 2). Inflammatory bowel disease–associated microbiota, such as Blautia, Helicobacter, and Ruminococcus, were changed in DSS-induced colitis after periodontitis salivary microbiota gavage. Periodontitis salivary microbiota decreased unsaturated fatty acid levels and increased arachidonic acid metabolism in DSS-induced colitis, which was positively correlated with Aerococcus and Ruminococcus, suggesting the key role of these metabolic events and microbes in the exacerbating effect of periodontitis salivary microbiota on experimental colitis. Our study demonstrated that periodontitis contributes to the pathogenesis of colitis through the swallowing of salivary microbiota, confirming the role of periodontitis in systemic disease and providing new insights into the etiology of gastrointestinal inflammatory diseases.

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“…In this study, we used NH 3 at a concentration of 25 ± 3 ppm to replicate the environmental stress and observed induction of both IL-1β and IL-10 as well as hemorrhage in the lung tissues. IL-1β and IL-10 are significant cytokines involved in regulating inflammatory response ( Li et al, 2016 ; Zhou et al, 2019 ; Shi et al, 2020 ). The results revealed that critical concentrations of NH 3 induced lung inflammation in broilers.…”

Section: Discussionmentioning

confidence: 99%

Dynamic Changes in Lung Microbiota of Broilers in Response to Aging and Ammonia Stress

et al. 2021

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Comprehensive microbial analysis has revealed that the lung harbors a complex variety of microbiota, and although the dynamic distribution of the lung microbiota in mice and laying hens of different ages is well established, this distribution has not been clarified in broilers of different ages. Here, we performed 16S rRNA gene sequencing of lung lavage fluid from broilers at 3 (3D), 7 (7D), 14 (14D), 21 (21D), and 35 (35D) days of age to evaluate changes in the composition of their lung microbiota. Upon examination of the composition and function of the broiler lung microbiota, we found that their maturation increased significantly with age. Specifically, the microbiota composition was similar between 7 and 14D and between 21 and 35D. The relative abundance of aerobic bacteria in the broiler lungs gradually increased as the broilers developed, whereas the relative abundance of potentially pathogenic bacteria reached its highest level at 3D. The relative abundance of predicted functions in microbiota was very similar among 3, 7, and 14D, whereas the Glycan Biosynthesis and Metabolism pathway in microbiota was enriched at 21D. These findings suggest that these metabolic pathways play critical roles in shaping broiler microbiota at these age stages. In addition, short-term external ammonia stimulation significantly increased lung inflammation but did not significantly affect the lung microbiota. Taken together, these data reveal the dynamics of age-related changes in the microbiota of broiler lungs and the stability (the significant variation in the microbial composition) of these microbial communities in response to short-term ammonia stress. These findings provide new insights into the development of broiler lung microbiota and serve as a reference for subsequent studies to evaluate disease prevention in broilers subjected to large-scale breeding.

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Intestinal vitamin D receptor knockout protects from oxazolone-induced colitis

Cited by 20 publications

References 31 publications

The Tryptophan Metabolite Indole-3-Carboxaldehyde Alleviates Mice with DSS-Induced Ulcerative Colitis by Balancing Amino Acid Metabolism, Inhibiting Intestinal Inflammation, and Improving Intestinal Barrier Function

The Tryptophan Metabolite Indole-3-Carboxaldehyde Alleviates Mice with DSS-Induced Ulcerative Colitis by Balancing Amino Acid Metabolism, Inhibiting Intestinal Inflammation, and Improving Intestinal Barrier Function

Periodontitis Salivary Microbiota Worsens Colitis

Dynamic Changes in Lung Microbiota of Broilers in Response to Aging and Ammonia Stress

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