Analysis of Intestinal Mucosa Integrity and GLP-2 Gene Functions upon Porcine Epidemic Diarrhea Virus Infection in Pigs

Zhou, Yajing; Ren, Zhanshi; Zhang, Shuai; Wang, Haifei; Wu, Shenglong; Bao, Wenbin

doi:10.3390/ani11030644

Cited by 4 publications

(3 citation statements)

References 29 publications

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“…According to the PEDV genome information, the fluorescent quantitative primers of M gene were designed ( Table S3 ), and the number of PEDV M gene cycles was detected by fluorescence quantitative analysis. The equation of the standard PEDV CV777 curve was established previously: y = −3.3354 lg(x) + 37.832, R2 = 0.9994, and the PEDV copy number was calculated [ 42 , 43 ].…”

Section: Methodsmentioning

confidence: 99%

m6A Demethylase ALKBH5 Restrains PEDV Infection by Regulating GAS6 Expression in Porcine Alveolar Macrophages

Jin

et al. 2022

IJMS

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Porcine epidemic diarrhea virus (PEDV) is a burdensome coronavirus for the global pig industry. Although its fecal-oral route has been well-recognized, increasing evidence suggests that PEDV can also spread through airborne routes, indicating that the infection may also occur in the respiratory tract. N6-methyladenosine (m6A) has been known to regulate viral replication and host immunity, yet its regulatory role and molecular mechanism regarding PEDV infection outside the gastrointestinal tract remain unexplored. In this study, we demonstrate that PEDV can infect porcine lung tissue and the 3D4/21 alveolar macrophage cell line, and the key m6A demethylase ALKBH5 is remarkably induced after PEDV infection. Interestingly, the disruption of ALKBH5 expression remarkably increases the infection’s capacity for PEDV. Transcriptome profiling identified dozens of putative targets of ALKBH5, including GAS6, which is known to regulate virus infectivity. Further, MeRIP-qPCR and mRNA stability analyses suggest that ALKBH5 regulates the expression of GAS6 via an m6A-YTHDF2-dependent mechanism. Overall, our study demonstrates that PEDV can infect porcine lung tissue and 3D4/21 cells and reveals the crucial role of ALKBH5 in restraining PEDV infections, at least partly, by influencing GAS6 through an m6A-YTHDF2-dependent mechanism.

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Section: Methodsmentioning

confidence: 99%

m6A Demethylase ALKBH5 Restrains PEDV Infection by Regulating GAS6 Expression in Porcine Alveolar Macrophages

Jin

et al. 2022

IJMS

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“…The IPEC-J2 cell line was initially isolated from the jejunum of newborn piglets and is composed of undifferentiated porcine intestinal crypt-based columnar cells [36]. According to previous studies, it can be confirmed that IPEC-J2 contains GLP2/GLP2R signal transduction [36][37][38], and importantly, Lgr5 + cells and other specialized IEC markers can be observed [39]. Based on the cell viability assay, the optimal concentration of SMP for IPEC-J2 cells was 0.3 mg/mL for 12 h (Fig.…”

Section: Inhibition Of Glp2/glp2r Signaling By Glp2 3−33 Disrupted Sm...mentioning

confidence: 99%

Role of the GLP2–Wnt1 axis in silicon-rich alkaline mineral water maintaining intestinal epithelium regeneration in piglets under early-life stress

Chen,

Dai,

Zhao

et al. 2024

Cell. Mol. Life Sci.

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Stress-induced intestinal epithelial injury (IEI) and a delay in repair in infancy are predisposing factors for refractory gut diseases in adulthood, such as irritable bowel syndrome (IBS). Hence, it is necessary to develop appropriate mitigation methods for mammals when experiencing early-life stress (ELS). Weaning, as we all know, is a vital procedure that all mammalian newborns, including humans, must go through. Maternal separation (MS) stress in infancy (regarded as weaning stress in animal science) is a commonly used ELS paradigm. Drinking silicon-rich alkaline mineral water (AMW) has a therapeutic effect on enteric disease, but the specific mechanisms involved have not been reported. Herein, we discover the molecular mechanism by which silicon-rich AMW repairs ELS-induced IEI by maintaining intestinal stem cell (ISC) proliferation and differentiation through the glucagon-like peptide (GLP)2–Wnt1 axis. Mechanistic study showed that silicon-rich AMW activates GLP2-dependent Wnt1/β-catenin pathway, and drives ISC proliferation and differentiation by stimulating Lgr5+ ISC cell cycle passage through the G1–S-phase checkpoint, thereby maintaining intestinal epithelial regeneration and IEI repair. Using GLP2 antagonists (GLP23−33) and small interfering RNA (SiWnt1) in vitro, we found that the GLP2–Wnt1 axis is the target of silicon-rich AMW to promote intestinal epithelium regeneration. Therefore, silicon-rich AMW maintains intestinal epithelium regeneration through the GLP2–Wnt1 axis in piglets under ELS. Our research contributes to understanding the mechanism of silicon-rich AMW promoting gut epithelial regeneration and provides a new strategy for the alleviation of ELS-induced IEI.

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“…Last but not least, GLP-2, a specific hormone that promotes intestinal growth, has been found to enhance the expression of tight junction proteins, facilitate mucosal repair, and improve the function of the intestinal barrier ( 30 – 32 ). Silencing the GLP-2 gene with shRNA transfection prior to infection has been shown to significantly increase the copies of PEDV in cells, indicating that a damaged barrier can facilitate PEDV infection ( 33 ).…”

Section: Microbes May Affect Pedv Infection Via Changed Intestinal Ba...mentioning

confidence: 99%

Mini-review: microbiota have potential to prevent PEDV infection by improved intestinal barrier

et al. 2023

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Porcine epidemic diarrhea virus (PEDV) infection poses a significant threat to the global pig industry. Current prevention and control strategies are inadequate in protecting pigs from new PEDV variants. This review aims to examine the relationship between PEDV and intestinal microbes, and investigate whether modulating intestinal microbes could affect PEDV infection. The mechanisms by which various intestinal microbes affect viral infection were initially introduced. Intestinal microbes can influence enteric viral infection through direct contact, such as binding, or by affecting interferons (IFNs) production and the intestinal barrier. Influencing the intestinal barrier by microbes can impact PEDV infection in young piglets. To narrow down the range of microbes that may influence PEDV infection, this review summarized microbes that change after infection. Short chain fatty acids (SCFAs), bacterial cell components, and toxins from microbes were identified as important mediators affecting PEDV infection. SCFAs primarily strengthen the intestinal barrier and inhibit intestinal inflammation, while bacterial cell components and toxins are more likely to damage the intestinal barrier. Therefore, this review hypothesizes that fecal transplantation, which allows the host to colonize more SCFAs-producing microbes, may prevent PEDV infection. However, these hypotheses require further proof, and the transplantation of intestinal microbes in pigs requires more exploration.

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Analysis of Intestinal Mucosa Integrity and GLP-2 Gene Functions upon Porcine Epidemic Diarrhea Virus Infection in Pigs

Cited by 4 publications

References 29 publications

m6A Demethylase ALKBH5 Restrains PEDV Infection by Regulating GAS6 Expression in Porcine Alveolar Macrophages

m6A Demethylase ALKBH5 Restrains PEDV Infection by Regulating GAS6 Expression in Porcine Alveolar Macrophages

Role of the GLP2–Wnt1 axis in silicon-rich alkaline mineral water maintaining intestinal epithelium regeneration in piglets under early-life stress

Mini-review: microbiota have potential to prevent PEDV infection by improved intestinal barrier

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