scholarly journals Effect of Puerarin, Baicalin and Berberine Hydrochloride on the Regulation of IPEC-J2 Cells Infected with Enterotoxigenic Escherichia coli

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Xiaoxi Liu ◽  
Fenghua Liu ◽  
Yunfei Ma ◽  
Huanrong Li ◽  
Xianghong Ju ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Bacterial Adhesion ◽  
Inflammatory Responses ◽  
Enterotoxigenic Escherichia Coli ◽  
Intestinal Epithelial ◽  
Berberine Hydrochloride ◽  
Main Components ◽  
Etec Infection

Puerarin, baicalin and berberine hydrochloride are the main components of Gegen Qinlian Decoction, which has been used to treat diarrhoea in China for hundreds of years, yet the biological function and molecular mechanism of these components are not clear. To investigate the effects of puerarin, baicalin, and berberine hydrochloride on the regulation of porcine intestinal epithelial cells (IPEC-J2 cells) infected with enterotoxigenic Escherichia coli (ETEC). IPEC-J2 cells were pretreated with puerarin (200 μg/mL), baicalin (1 μg/mL), and berberine hydrochloride (100 μg/mL) at 37°C for 3 h and then coincubated with the F4ac ETEC bacterial strain 200 at 37°C for 3 h. ETEC infection damaged the structure of IPEC-J2 cells, upregulated mucin 4 (P < 0.01) and mucin 13 mRNA (P < 0.05) expression, increased the apoptosis rate (P < 0.05), and promoted inflammatory responses (IL-6 and CXCL-2 mRNA expression) in IPEC-J2 cells by activating the nuclear factor-κB (NF-κB) signaling pathway. Pretreatment with puerarin, baicalin, and berberine hydrochloride improved the structure and morphology of IPEC-J2 cells and inhibited ETEC adhesion by downregulating specific adhesion molecules. Pretreatment with baicalin decreased the inflammatory response; pretreatment with baicalin and berberine hydrochloride decreased the inflammatory response mediated by the NF-κB signaling pathway. Pretreatment with puerarin, baicalin, and berberine hydrochloride protected IPEC-J2 cells from ETEC infection by inhibiting bacterial adhesion and inflammatory responses.

scholarly journals Enterotoxigenic Escherichia coli infection and intestinal thiamin uptake: studies with intestinal epithelial Caco-2 monolayers

2013 ◽  
Vol 305 (11) ◽  
pp. C1185-C1191 ◽  
Author(s):  
Abhisek Ghosal ◽  
Nabendu S. Chatterjee ◽  
Tristan Chou ◽  
Hamid M. Said
Keyword(s):  
Escherichia Coli ◽  
Significant Inhibition ◽  
Water Soluble ◽  
Enterotoxigenic Escherichia Coli ◽  
Adenylate Cyclase System ◽  
Mrna Levels ◽  
Intestinal Epithelial ◽  
E Coli ◽  
Heat Labile ◽  
Etec Infection

Infections with enteric pathogens like enterotoxigenic Escherichia coli ( ETEC) is a major health issue worldwide and while diarrhea is the major problem, prolonged, severe, and dual infections with multiple pathogens may also compromise the nutritional status of the infected individuals. There is almost nothing currently known about the effect of ETEC infection on intestinal absorptions of water-soluble vitamins including thiamin. We examined the effect of ETEC infection on intestinal uptake of the thiamin using as a model the human-derived intestinal epithelial Caco-2 cells. The results showed that infecting confluent Caco-2 monolayers with live ETEC (but not with boiled/killed ETEC or nonpathogenic E. coli) or treatment with bacterial culture supernatant led to a significant inhibition in thiamin uptake. This inhibition appears to be caused by a heat-labile and -secreted ETEC component and is mediated via activation of the epithelial adenylate cyclase system. The inhibition in thiamin uptake by ETEC was associated with a significant reduction in expression of human thiamin transporter-1 and -2 (hTHTR1 and hTHTR2) at the protein and mRNA levels as well as in the activity of the SLC19A2 and SLC19A3 promoters. Dual infection of Caco-2 cells with ETEC and EPEC (enteropathogenic E. coli) led to compounded inhibition in intestinal thiamin uptake. These results show for the first time that infection of human intestinal epithelial cells with ETEC causes a significant inhibition in intestinal thiamin uptake. This inhibition is mediated by a secreted heat-labile toxin and is associated with a decrease in the expression of intestinal thiamin transporters.

scholarly journals Lasso Peptide Microcin J25 Effectively Enhances Gut Barrier Function and Modulates Inflammatory Response in an Enterotoxigenic Escherichia coli-Challenged Mouse Model

2020 ◽  
Vol 21 (18) ◽  
pp. 6500 ◽  
Author(s):  
Xiuliang Ding ◽  
Haitao Yu ◽  
Shiyan Qiao
Keyword(s):  
Escherichia Coli ◽  
Barrier Function ◽  
Inflammatory Responses ◽  
Intestinal Morphology ◽  
Enterotoxigenic Escherichia Coli ◽  
Control Group ◽  
Lasso Peptide ◽  
Gut Barrier Function ◽  
Microcin J25 ◽  
Etec Infection

Bacterial resistance leads to severe public health and safety issues worldwide. Alternatives to antibiotics are currently needed. A promising lasso peptide, microcin J25 (MccJ25), is considered to be the best potential substitute for antibiotics to treat pathogen infection, including enterotoxigenic Escherichia coli (ETEC). This study evaluated the efficacy of MccJ25 in the prevention of ETEC infection. Forty-five female BALB/c mice of clean grade (aged seven weeks, approximately 16.15 g) were randomly divided into three experimental groups as follows: (i) control group (uninfected); (ii) ETEC infection group; (iii) MccJ25 + ETEC group. Fifteen mice per group in five cages, three mice/cage. MccJ25 conferred effective protection against ETEC-induced body weight loss, decrease in rectal temperature and increase in diarrhea scores in mice. Moreover, in ETEC-challenged mice model, MccJ25 significantly improved intestinal morphology, decreased intestinal histopathological scores and attenuated intestinal inflammation by decreasing proinflammatory cytokines and intestinal permeability, including reducing serum diamine oxidase and D-lactate levels. MccJ25 enhanced epithelial barrier function by increasing occludin expression in the colon and claudin-1 expression in the jejunum, ultimately improving intestinal health of host. MccJ25 was further found to alleviate gut inflammatory responses by decreasing inflammatory cytokine production and expression via the activation of the mitogen-activated protein kinase and nuclear factor κB signaling pathways. Taken together, the results indicated that MccJ25 protects against ETEC-induced intestinal injury and intestinal inflammatory responses, suggesting the potential application of MccJ25 as an excellent antimicrobial or anti-inflammation agent against pathogen infections.

scholarly journals Contribution of the Highly Conserved EaeH Surface Protein to Enterotoxigenic Escherichia coli Pathogenesis

2014 ◽  
Vol 82 (9) ◽  
pp. 3657-3666 ◽  
Author(s):  
Alaullah Sheikh ◽  
Qingwei Luo ◽  
Koushik Roy ◽  
Salwa Shabaan ◽  
Pardeep Kumar ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Bacterial Adhesion ◽  
Surface Protein ◽  
Enterotoxigenic Escherichia Coli ◽  
Intestinal Epithelial ◽  
Content Type ◽  
Common Causes ◽  
Colonization Factors ◽  
Fimbrial Adhesins ◽  
Substantial Morbidity

ABSTRACTEnterotoxigenicEscherichia coli(ETEC) strains are among the most common causes of diarrheal illness worldwide. These pathogens disproportionately afflict children in developing countries, where they cause substantial morbidity and are responsible for hundreds of thousands of deaths each year. Although these organisms are important targets for enteric vaccines, most development efforts to date have centered on a subset of plasmid-encoded fimbrial adhesins known as colonization factors and heat-labile toxin (LT). Emerging data suggest that ETEC undergoes considerable changes in its surface architecture, sequentially deploying a number of putative adhesins during its interactions with the host. We demonstrate here that one putative highly conserved, chromosomally encoded adhesin, EaeH, engages the surfaces of intestinal epithelial cells and contributes to bacterial adhesion, LT delivery, and colonization of the small intestine.

scholarly journals Enterotoxigenic Escherichia coli Modulates Host Intestinal Cell Membrane Asymmetry and Metabolic Activity

2008 ◽  
Vol 77 (1) ◽  
pp. 341-347 ◽  
Author(s):  
Amber M. Johnson ◽  
Radhey S. Kaushik ◽  
Nicholas J. Rotella ◽  
Philip R. Hardwidge
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Regulatory Region ◽  
Host Cells ◽  
Enterotoxigenic Escherichia Coli ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Membrane Asymmetry ◽  
Induced Apoptosis ◽  
Etec Infection

ABSTRACT Enterotoxigenic Escherichia coli (ETEC) is a common cause of travelers' and postweaning diarrhea in humans and swine, respectively. The extent to which ETEC damages host cells is unclear. Experiments are presented that probe the ability of porcine ETEC isolates to induce apoptosis and cell death in porcine intestinal epithelial cells. Quantification of host phosphatidylserine exposure following ETEC infection suggested that ETEC induced changes in plasma membrane asymmetry, independent of the expression of the heat-labile enterotoxin. Significant host cell death was not observed. ETEC infection also caused a drastic inhibition of host esterase activity, as measured by calcein fluorescence. While ETEC infection resulted in activation of host caspase 3, terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling of DNA double-strand breakage, indicative of late stages of apoptosis, was not observed. Camptothecin-induced apoptosis markedly increased subsequent ETEC adherence. Transfer of cell-free supernatants from apoptotic cells to bacterial inocula prior to infection of naïve cells increased the transcriptional activity of the regulatory region upstream of the K88ac operon and promoted subsequent adherence to host cells.

Zinc oxide inhibits enterotoxigenic Escherichia coli K88 growth in culture and reduces the inflammatory response of porcine intestinal epithelial cells to infection

2009 ◽  
Vol 2009 ◽  
pp. 32-32
Author(s):  
H Sargeant ◽  
M-A Shaw ◽  
H M Miller
Keyword(s):  
Escherichia Coli ◽  
Zinc Oxide ◽  
Intestinal Epithelial Cells ◽  
Innate Immune ◽  
Enterotoxigenic Escherichia Coli ◽  
Intestinal Cells ◽  
Intestinal Epithelial ◽  
Genomic Study ◽  
Etec Infection

Pharmacological levels of zinc oxide in the post-weaning piglet diet reduce the incidence and severity of diarrhoea, in particular that caused by enterotoxigenic Escherichia coli (ETEC) K88 (Owusu-Asiedu et al. 2003). A previous in vivo genomic study (Sargeant et al, 2008) identified several genes differentially expressed in the small intestine of ETEC-challenged piglets when fed a zinc oxide-supplemented diet. This included decreased expression of several genes involved in the inflammatory and innate immune response. It has been reported that ZnO reduces adhesion and internalisation of K88 to cultured human enterocytes, counteracting the up-regulation of inflammatory cytokines caused by ETEC infection. However, this effect was not due to growth inhibition of ETEC K88 in ZnO (Roselli et al, 2003). The objective of this study was to determine whether zinc oxide shows the same mode of action in protecting porcine intestinal cells against ETEC K88 as has been demonstrated in human cells, providing an explanation for in vivo findings.

scholarly journals Bacteriophage EK99P-1 Alleviates Enterotoxigenic Escherichia Coli K99-Induced Barrier Dysfunction and Inflammation

2021 ◽  
Author(s):  
Narae Kim ◽  
Min jeong Gu ◽  
Yoon-Chul Kye ◽  
Young-Jun Ju ◽  
Rira Hong ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Enterotoxigenic Escherichia Coli ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Peripheral Blood Mononuclear ◽  
Barrier Disruption ◽  
Basolateral Side

Abstract Background Bacteriophages have long been used as a potential alternative to antibiotics for livestock due to their ability to specifically kill enterotoxigenic Escherichia coli (ETEC), which are a major cause of diarrhea in piglets. However, the control of ETEC infection by phages within intestinal epithelial cells, and their relationship with host immune responses, remain poorly understood. Results In this study, we evaluated the effect of phage EK99P-1 against ETEC K99-infected porcine intestinal epithelial cell line (IPEC-J2). Phage EK99P-1 prevented ETEC K99-induced barrier disruption by attenuating the increased permeability mediated by the loss of tight junction proteins such as zonula occludens-1 (ZO-1), occludin, and claudin-3. ETEC K99-induced inflammatory responses, such as IL-8 secretion, were decreased by treatment with phage EK99P-1. We used a IPEC-J2/peripheral blood mononuclear cell (PBMC) Transwell co-culture system to investigate whether the modulation of barrier disruption and chemokine secretion by phage EK99P-1 in ETEC K99-infected IPEC-J2 would influence basolateral immune cells. The results showed that phage EK99P-1 reduced the mRNA expression of ETEC K99-induced pro-inflammatory cytokines, interleukin (IL)-1β and IL-8, from pPBMC collected on the basolateral side. Conclusion Together, these results suggest that phage EK99P-1 prevented ETEC K99-induced barrier dysfunction in IPEC-J2 and alleviated inflammation caused by ETEC K99 infection. Reinforcement of the intestinal barrier by phage EK99P-1 also modulates the immune cell inflammatory response.

scholarly journals Deletion of FaeG alleviated Enterotoxigenic Escherichia coli F4ac-induced apoptosis in the intestine

AMB Express ◽  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Pengpeng Xia ◽  
Yunping Wu ◽  
Siqi Lian ◽  
Guomei Quan ◽  
Yiting Wang ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Clinical Symptoms ◽  
Mucosal Damage ◽  
Enterotoxigenic Escherichia Coli ◽  
Intestinal Epithelial ◽  
Antibody Microarray ◽  
E Coli ◽  
Fimbrial Subunit ◽  
Induced Apoptosis ◽  
Weaning Piglets

AbstractEnterotoxigenic Escherichia coli (ETEC) F4ac is a major constraint to the development of the pig industry, which is causing newborn and post-weaning piglets diarrhea. Previous studies proved that FaeG is the major fimbrial subunit of F4ac E. coli and efficient for bacterial adherence and receptor recognition. Here we show that the faeG deletion attenuates both the clinical symptoms of F4ac infection and the F4ac-induced intestinal mucosal damage in piglets. Antibody microarray analysis and the detection of mRNA expression using porcine neonatal jejunal IPEC-J2 cells also determined that the absence of FaeG subunit alleviated the F4ac promoted apoptosis in the intestinal epithelial cells. Thus, targeted depletion of FaeG is still beneficial for the prevention or treatment of F4ac infection.

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