New Insight into the Molecular Mechanism of the FUT2 Regulating Escherichia coli F18 Resistance in Weaned Piglets

Wu, Zhengchang; Feng, Hanping; Cao, Yue; Huang, Yanjie; Dai, Chaohui; Wu, Shenglong; Bao, Wenbin

doi:10.3390/ijms19113301

Cited by 18 publications

(15 citation statements)

References 47 publications

(56 reference statements)

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“…In Sutai Escherichia coli F18-sensitive and resistant pigs, FUT2 methylation changes at the mC-6 and mC-22 sites were significantly negatively correlated with FUT2 mRNA expression level. Furthermore, methylation at the mC-22 site inhibited the binding of Sp1 to the FUT2 promoter, thereby reducing FUT2 expression and enhancing resistance to E. coli F18 in weaned piglets [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Regulatory Effect of Methylation of the Porcine AQP3 Gene Promoter Region on Its Expression Level and Porcine Epidemic Diarrhea Virus Resistance

Jia

Wang

et al. 2020

Genes

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As an important carrier for intestinal secretion and water absorption, aquaporin 3 (AQP3) is closely related to diarrhea. In this study, we investigated the mechanisms of AQP3 gene expression regulation in porcine epidemic diarrhea virus (PEDV)-induced diarrhea confirmed by PCR amplification and sequencing. Evaluation of intestinal pathology showed that diarrhea caused by PEDV infection destroyed the intestinal barrier of piglets. qPCR analysis showed that AQP3 expression in the small intestine of PEDV-infected piglets was extremely significantly decreased. qPCR and Bisulfite sequencing PCR revealed an increase in the methylation levels of both CpG islands in the AQP3 promoter region in the jejunum of PEDV-infected piglets. The methylation of mC-20 and mC-10 sites within the two CpG islands showed a significant negative correlation with AQP3 expression. Chromatin Co-Immunoprecipitation (ChIP)-PCR showed that the Sp1 transcription factor was bound to the AQP3 promoter region containing these two CpG sites. AQP3 expression was also extremely significantly reduced in Sp1-inhibited IPEC-J2 cells, indicating that abnormal methylation at the mC-20 site of CpG1 and the mC-10 site of CpG2 reduces its expression in PEDV-infected piglet jejunum by inhibiting the binding of Sp1 to the AQP3 promoter. These findings provide a theoretical basis for further functional studies of porcine AQP3.

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Section: Introductionmentioning

confidence: 99%

Regulatory Effect of Methylation of the Porcine AQP3 Gene Promoter Region on Its Expression Level and Porcine Epidemic Diarrhea Virus Resistance

Jia

Wang

et al. 2020

Genes

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“…Similar observations have been found for non-secretors in association with antibiotic susceptibility. 25,[65][66] We did not find much cross-reference linking AMR and AKI, with blood group secretor status. This is an important observation requiring further study in a larger subset.…”

Section: Discussionmentioning

confidence: 56%

Predisposition of Blood group Non-secretors to Urinary tract infection with Escherichia coli Anti-microbial Resistance and Acute Kidney Injury

Thiagarajan¹,

Spellman²,

Kanagamuthu³

et al. 2021

J. Pure Appl. Microbiol.

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Urinary tract infection (UTI) causes significant renal damage and disease severity is compounded by antimicrobial resistance (AMR) and other comorbidities in the patient. Blood group antigens secreted in body fluids (secretor status) are known to play a role in bacterial adhesion and we studied its influence on AMR in UTI. A total of 2758 patients with UTI were studied with urine culture, qualitative and semiquantitative urine microscopy, serum creatinine and secretor status in saliva samples by adsorption-inhibition method. Of these, AMR from 300 patients with E. coli infection were assessed as per CLSI 2019 guidelines and extended-spectrum beta-lactamase (ESBL) genes (bla TEM, bla CTX-M, bla SHV) and NDM1 genes were studied using TaqMan probes in Real-time polymerase chain reaction. Patients with UTI were followed up for two weeks. Female patients had higher predilection (57%) for E. coli infection while patients with diabetes or non-secretors had none. In our study, ESBL producers were seen in 62% of the E. coli isolates and fosfomycin had 100% susceptibility. Non-secretors were significantly associated with acute kidney injury (AKI), AMR and ESBL genes. Multidrug-resistant (MDR) was noted in 127/160 (79.4%) ESBL and 17/18 (94%) NDM1 gene encoding strains. Quantitative urine microscopy scoring predicted AKI both at presentation and at end of follow up. ESBL producers were common in our study population and non-secretors had a significant association with AMR genes. Urine microscopy scoring system may be a useful tool to predict AKI in patients with UTI.

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“…As such, we stimulated PK15 cells with LPS or with porcine E. coli F18, revealing that both of these treatments resulted in significant BPI upregulation. Glycosphingolipid biosynthesis-globo series pathway genes ( FUT1 , FUT2 ) are involved in the formation of the E. coli F18 receptor, and its expression level is closely related to resistance to E. coli F18 in piglets [ 28 , 29 ]. TLRs recognize different microbial components, sense microbial populations in the intestinal tract, initiate proinflammatory signaling pathways to resist the invasion of pathogenic microorganisms and play an important role in immune regulation in the process of resisting E. coli F18 infection [ 30 , 31 ].…”

Section: Discussionmentioning

confidence: 99%

The Impact of BPI Expression on Escherichia coli F18 Infection in Porcine Kidney Cells

Jin

Huang

Sun

et al. 2020

Animals

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The efficacy and regulatory activity of bactericidal/permeability-increasing protein (BPI) as a mediator of Escherichia coli (E. coli) F18 resistance remains to be defined. In the present study, we evaluated lipopolysaccharide (LPS)-induced changes in BPI gene expression in porcine kidney (PK15) cells in response to E. coli F18 exposure. We additionally generated PK15 cells that overexpressed BPI to assess the impact of this gene on Toll-like receptor 4 (TLR4) signaling and glycosphingolipid biosynthesis-related genes. Through these analyses, we found that BPI expression rose significantly following LPS exposure in response to E. coli F18ac stimulation (p < 0.01). Colony count assays and qPCR analyses revealed that E. coli F18 adherence to PK15 cells was markedly suppressed following BPI overexpression (p < 0.01). BPI overexpression had no significant effect on the mRNA-level expression of genes associated with glycosphingolipid biosynthesis or TLR4 signaling. BPI overexpression suppressed the LPS-induced TLR4 signaling pathway-related expression of proinflammatory cytokines (IFN-α, IFN-β, MIP-1α, MIP-1β and IL-6). Overall, our study serves as an overview of the association between BPI and resistance to E. coli F18 at the cellular level, offering a framework for future investigations of the mechanisms whereby piglets are able to resist E. coli F18 infection.

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New Insight into the Molecular Mechanism of the FUT2 Regulating Escherichia coli F18 Resistance in Weaned Piglets

Cited by 18 publications

References 47 publications

Regulatory Effect of Methylation of the Porcine AQP3 Gene Promoter Region on Its Expression Level and Porcine Epidemic Diarrhea Virus Resistance

Regulatory Effect of Methylation of the Porcine AQP3 Gene Promoter Region on Its Expression Level and Porcine Epidemic Diarrhea Virus Resistance

Predisposition of Blood group Non-secretors to Urinary tract infection with Escherichia coli Anti-microbial Resistance and Acute Kidney Injury

The Impact of BPI Expression on Escherichia coli F18 Infection in Porcine Kidney Cells

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