Autophagy and Gastrointestinal Diseases

Wang, Tao; Liu, Kewei; Wen, Liangzhi; Yang, Yang; Yin, Xinru; Liu, Kaijun; Chen, Yuqin; He, Yu-Qin; Ye, Min; Wei, Yanling; Wang, Bin; Chen, Dongfeng

doi:10.1007/978-981-15-4272-5_38

Cited by 20 publications

(14 citation statements)

References 17 publications

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“…By using whole-exome sequencing of familial forms of sarcoidosis, our group identified mutations in genes encoding essential factors for autophagy regulation, for example, the mTOR and Rac1 (Ras-related C3 botulinum toxin substrate 1) molecular hubs, we posited that this predisposing state might be related to constitutional defects in the regulation of macroautophagy – a crucial process allowing the clearance of any microbial and nonmicrobial particles [ 4 ]. Similar mechanisms have been suggested for other granulomatous and inflammatory disorders such as Crohn’s disease [ 5 ]. Whether patients with sarcoidosis present differential susceptibility to SARS-CoV-2 infection remains unknown; however, several projects have been initiated to address this question [ 6 ].…”

Section: From Covid-19 To Sarcoidosissupporting

confidence: 69%

Modeling Potential Autophagy Pathways in COVID-19 and Sarcoidosis

Calender

Israël‐Biet

Valeyre

et al. 2020

Trends in Immunology

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Section: From Covid-19 To Sarcoidosissupporting

confidence: 69%

Modeling Potential Autophagy Pathways in COVID-19 and Sarcoidosis

Calender

Israël‐Biet

Valeyre

et al. 2020

Trends in Immunology

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“…GC comprises the following precancerous steps: chronic active gastritis → chronic atrophic gastritis → gastric intestinal metaplasia → gastric epithelial dysplasia [ 18 ]. Inflammation, cell proliferation and apoptosis, autophagy dysfunction, energy metabolism disorders, and other factors may contribute to the development process, although the exact pathogenesis is still unclear [ 14 , 17 , 19 , 20 ]. The common therapies used for CAG focus on symptomatic treatment and are often not completely effective.…”

Section: Discussionmentioning

confidence: 99%

16S rRNA sequencing-based evaluation of the protective effects of Hua-Zhuo-Jie-Du on rats with chronic atrophic gastritis

Zhou

Yang

Xu³

et al. 2022

BMC Complement Med Ther

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Background Disturbance of the intestinal flora is a pathogenic factor for chronic atrophic gastritis (CAG). Hua-Zhuo-Jie-Du (HZJD) has been shown to be an effective Chinese herbal preparation for treating CAG. However, the effects of HZJD on the intestinal flora of CAG is unclear. In this study, we probed the regulating effects of HZJD on intestinal microbes in CAG rats using 16S rRNA gene sequencing. Methods High-performance liquid chromatography (HPLC) analysis was used to perform quality control of HZJD preparations. We then administered 1-methyl-3-nitro-1-nitrosoguanidine (200 μg/ml) to Sprague–Dawley rats to establish a CAG model. HZJD and vitacoenzyme were administered orally to these rats over a 10 week period. Hematoxylin and eosin (H&E) staining was performed to observe the histopathology of CAG rats. A rarefaction curve, species accumulation curve, Chao1 index, and ACE index were calculated to assess the alpha diversity. Principal component analysis (PCA), non-metric multi-dimensional scaling (NMDS), and unweighted pair group method with arithmetic mean (UPGMA) were conducted to examine the beta diversity. The LEfSe method was used to identify differential bacteria. Differential function analysis used PCA based on KEGG function prediction. Results HPLC showed that our HZJD preparation method was feasible. H&E staining showed that HZJD significantly improved the pathological state of the gastric mucosa in CAG rats. The rarefaction curve and species accumulation curve showed that the sequencing data were reasonable. The Chao1 and ACE indices were significantly increased in CAG rats compared to the N group. Following HZJD and vitacoenzyme treatment, the Chao1 and ACE indices were decreased. PCA, NMDS, and UPGMA results showed that the M group was separated from the N, HZJD, and V groups, and LEfSe results showed that the relative abundance of Akkermansia, Oscillospira, Prevotella, and CF231 were significantly higher in the N group. Proteobacteria and Escherichia were significantly enriched in the M group, Allobaculum, Bacteroides, Jeotgalicoccus, Corynebacterium, and Sporosarcina were significantly enriched in the V group, and Firmicutes, Lactobacillus, and Turicibacter were significantly enriched in the HZJD group. Conclusion HZJD exhibited a therapeutic effect on the intestinal flora of CAG rats.

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“…It is also an essential component of immune defense against bacterial pathogens such as Mycobacterium tuberculosis , Salmonella enteric , and Escherichia coli [ 19 , 20 , 21 ]. Thus, triggering autophagy is essential for cell survival during pathogen infection [ 22 , 23 ]. The induction of autophagy involves numerous proteins and multiple signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Gliadin Peptide P31-43 Induces mTOR/NFkβ Activation and Reduces Autophagy: The Role of Lactobacillus paracasei CBA L74 Postbiotc

Conte¹,

Nigro²,

Porpora³

et al. 2022

IJMS

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Celiac disease (CD) is an autoimmune disease characterized by an altered immune response stimulated by gliadin peptides that are not digested and cause damage to the intestinal mucosa. The aim of this study was to investigate whether the postbiotic Lactobacillus paracasei (LP) could prevent the action of gliadin peptides on mTOR, autophagy, and the inflammatory response. Most of the experiments performed were conducted on intestinal epithelial cells Caco-2 treated with a peptic-tryptic digest of gliadin (PTG) and P31-43. Furthermore, we pretreated the Caco-2 with the postbiotic LP before treatment with the previously described stimuli. In both cases, we evaluated the levels of pmTOR, p70S6k, and p4EBP-1 for the mTOR pathway, pNFkβ, and pERK for inflammation and LC 3 and p62 for autophagy. For autophagy, we also used immunofluorescence analysis. Using intestinal organoids derivate from celiac (CD) patients, we analyzed the effect of gliadin after postbiotic pretreatment with LP on inflammation marker NFkβ. Through these experiments, we showed that gliadin peptides are able to induce the increase of the inflammatory response in a more complex model of intestinal epithelial cells. LP postbiotic was able to induce autophagy in Caco-2 cells and prevent gliadin effects. In conclusion, postbiotic pretreatment with LP could be considered for in vivo clinical trials.

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Autophagy and Gastrointestinal Diseases

Cited by 20 publications

References 17 publications

Modeling Potential Autophagy Pathways in COVID-19 and Sarcoidosis

Modeling Potential Autophagy Pathways in COVID-19 and Sarcoidosis

16S rRNA sequencing-based evaluation of the protective effects of Hua-Zhuo-Jie-Du on rats with chronic atrophic gastritis

Gliadin Peptide P31-43 Induces mTOR/NFkβ Activation and Reduces Autophagy: The Role of Lactobacillus paracasei CBA L74 Postbiotc

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