Effects of HSP27 gene expression on the resistance to Escherichia coli infection in piglets

Zong, Qiufang; Jing, Pengfei; Sun, Shengyuan; Wang, Haifei; Wu, Shenglong; Bao, Wenbin

doi:10.1016/j.gene.2021.145415

Cited by 4 publications

(2 citation statements)

References 32 publications

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“…While expression of HSP25/27 and HSP70 has been associated with enhanced anti-inflammatory cytokine IL-10 production in macrophages, DCs, and regulatory T cells, respectively ( 15 , 39 ). It is also reported that overexpression of HSP27 gene facilitates the porcine epithelium to resist Escherichia coli infection in vitro ( 40 ).…”

Section: Discussionmentioning

confidence: 99%

Epithelial Heat Shock Proteins Mediate the Protective Effects of Limosilactobacillus reuteri in Dextran Sulfate Sodium-Induced Colitis

Liu

Zhu

et al. 2022

Front. Immunol.

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Defects in gut barrier function are implicated in gastrointestinal (GI) disorders like inflammatory bowel disease (IBD), as well as in systemic inflammation. With the increasing incidence of IBD worldwide, more attention should be paid to dietary interventions and therapeutics with the potential to boost the natural defense mechanisms of gut epithelial cells. The current study aimed to investigate the protective effects of Limosilactobacillus reuteri ATCC PTA 4659 in a colitis mouse model and delineate the mechanisms behind it. Wild-type mice were allocated to the control group; or given 3% dextran sulfate sodium (DSS) in drinking water for 7 days to induce colitis; or administered L. reuteri for 7 days as pretreatment; or for 14 days starting 7 days before subjecting to the DSS. Peroral treatment with L. reuteri improved colitis severity clinically and morphologically and reduced the colonic levels of Tumor necrosis factor-α (TNF-α) (Tnf), Interleukin 1-β (Il1β), and nterferon-γ (Ifng), the crucial pro-inflammatory cytokines in colitis onset. It also prevented the CD11b+Ly6G+ neutrophil recruitment and the skewed immune responses in mesenteric lymph nodes (MLNs) of CD11b+CD11c+ dendritic cell (DC) expansion and Foxp3+CD4+ T-cell reduction. Using 16S rRNA gene amplicon sequencing and RT-qPCR, we demonstrated a colitis-driven bacterial translocation to MLNs and gut microbiota dysbiosis that were in part counterbalanced by L. reuteri treatment. Moreover, the expression of barrier-preserving tight junction (TJ) proteins and cytoprotective heat shock protein (HSP) 70 and HSP25 was reduced by colitis but boosted by L. reuteri treatment. A shift in expression pattern was also observed with HSP70 in response to the pretreatment and with HSP25 in response to L. reuteri-DSS. In addition, the changes of HSPs were found to be correlated to bacterial load and epithelial cell proliferation. In conclusion, our results demonstrate that the human-derived L. reuteri strain 4659 confers protection in experimental colitis in young mice, while intestinal HSPs may mediate the probiotic effects by providing a supportive protein–protein network for the epithelium in health and colitis.

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Section: Discussionmentioning

confidence: 99%

Epithelial Heat Shock Proteins Mediate the Protective Effects of Limosilactobacillus reuteri in Dextran Sulfate Sodium-Induced Colitis

Liu

Zhu

et al. 2022

Front. Immunol.

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“…In general, the intestinal porcine epithelial cell (IPEC-J2) is an efficient cell model for the examination of the underlying mechanism behind the host anti- E. coli F18 pathogen [ 7 , 20 ]. In addition, multiple studies have revealed that the IPEC-J2 exposure to E. coli triggers oxidative damage and inflammatory responses, which results in enhancing apoptotic cell death and diminishing functionality [ 21 , 22 , 23 ].…”

Section: Introductionmentioning

confidence: 99%

Comprehensive Analysis Revealed the Potential Roles of N6-Methyladenosine (m6A) Mediating E. coli F18 Susceptibility in IPEC-J2 Cells

Wang

et al. 2022

IJMS

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Post-weaning diarrhea caused by enterotoxigenic Escherichia coli F18 (E. coli F18) causes significant economic losses for pig producers. N6-methyladenosine (m6A) is a highly abundant epitranscriptomic marker that has been found to be involved in regulating the resistance of host cells to pathogenic infection, but its potential role in E. coli F18-exposed intestinal porcine epithelial cells (IPEC-J2) remains undetermined. Here, we demonstrated that m6A and its regulators modulate E. coli F18 susceptibility. Briefly, we revealed that the Wilms’ tumor 1-associating protein (WTAP) expressions were markedly elevated in IPEC-J2 cells upon E. coli F18 exposure. WTAP are required for the regulation of E. coli F18 adhesion in IPEC-J2 cells. Additionally, WTAP knockdown significantly suppressed m6A level at N-acetyllactosaminide beta-1,6-N-acetylglucosaminyl-transferase (GCNT2) 3′UTR, resulting in the enhancement of TH N6-methyladenosine RNA binding protein 2 (YTHDF2)-mediated GCNT2 mRNA stability. Subsequently, the altered GCNT2 expressions could inhibit the glycosphingolipid biosynthesis, thus improving resistance to E. coli F18 infection in IPEC-J2. Collectively, our analyses highlighted the mechanism behind the m6A-mediated management of E. coli F18 susceptibility, which will aid in the development of novel approaches that protect against bacterial diarrhea in piglets.

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METTL3 enhances E. coli F18 resistance by targeting IKBKG/NF-κB signaling via an m6A-YTHDF1–dependent manner in IPEC-J2 cells

Jin,

Liu,

et al. 2024

International Journal of Biological Macromolecules

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Effects of HSP27 gene expression on the resistance to Escherichia coli infection in piglets

Cited by 4 publications

References 32 publications

Epithelial Heat Shock Proteins Mediate the Protective Effects of Limosilactobacillus reuteri in Dextran Sulfate Sodium-Induced Colitis

Epithelial Heat Shock Proteins Mediate the Protective Effects of Limosilactobacillus reuteri in Dextran Sulfate Sodium-Induced Colitis

Comprehensive Analysis Revealed the Potential Roles of N6-Methyladenosine (m6A) Mediating E. coli F18 Susceptibility in IPEC-J2 Cells

METTL3 enhances E. coli F18 resistance by targeting IKBKG/NF-κB signaling via an m6A-YTHDF1–dependent manner in IPEC-J2 cells

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