Effects of the lipid-coated zinc oxide dietary supplement on intestinal mucosal morphology and gene expression associated with the gut health in weanling pigs challenged with enterotoxigenic Escherichia coli K88

2018 ◽  
Vol 98 (3) ◽  
pp. 538-547 ◽  
Author(s):  
Jeong Hee Han ◽  
Min Hye Song ◽  
Ha Na Kim ◽  
Insurk Jang ◽  
C. Young Lee ◽  
...  

Effects of a lipid-coated zinc oxide (ZnO) Shield Zn® (SZ) vs. ZnO were evaluated. Forty 25-d-old weanling pigs were fed a nursery diet supplemented with 100 mg kg−1 Zn with ZnO (ZnO-100), ZnO-2500, SZ-100, -200, or -400. All piglets were challenged orally with 5 × 108 colony-forming units of enterotoxigenic Escherichia coli K88 on day 7 and euthanized on day 14. The fecal consistency score (FCS) was less for the SZ group vs. ZnO-100 (P < 0.05). The intestinal villus height:crypt depth ratio and goblet cell density were greater for the SZ group vs. ZnO-100. By regression analyses, SZ-100 to -200 and SZ-300 to -400 were comparable to ZnO-2500 in the FCS and intestinal variables, respectively. The jejunal mucosal mRNA level did not differ between the SZ group and either ZnO group in insulin-like growth factor-I and multiple structural proteins and cytokines including zonula occludens protein (ZO) 1 and interleukin (IL) 10 except for lower ZO-1 and IL-10 mRNA levels for the SZ group than for ZnO-2500 and ZnO-100, respectively. The ZO-1 mRNA level regressed positively on the supplemental SZ concentration. Results suggest that SZ play a role in epithelial barrier function and inflammation by modulating the expression of ZO-1 and IL-10.

2013 ◽  
Vol 305 (11) ◽  
pp. C1185-C1191 ◽  
Author(s):  
Abhisek Ghosal ◽  
Nabendu S. Chatterjee ◽  
Tristan Chou ◽  
Hamid M. Said

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.


2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 84-85
Author(s):  
Sue Sinn ◽  
Ran Song ◽  
Dana Beckler ◽  
Rob Musser ◽  
Kim Friesen

Abstract A mineral-based feed additive, NutriQuest Protect™, was evaluated in five artificial Enterotoxigenic Escherichia coli (ETEC) challenge experiments to determine the effects on pig growth performance, fecal consistency and immune response. The five experiments were conducted following a similar procedure and utilized a total of 232 weanling pigs (19 d of age) assigned to one of three experimental treatments: non-challenged control (NC), challenged control (CC), and challenged pigs fed Protect at 4.0 g/kg (CP) with 36, 36, and 44 pens per treatment, respectively. Pharmacological ZnO or medications were not included in any diets. Pigs were allowed a 7-d adaptation period following weaning, orally inoculated with E. coli K88 or F18 on 0 d post-inoculation (dpi) and 1-dpi. Studies were concluded on 4-dpi. Pig BW and feed disappearance were measured on 0-dpi and 4-dpi. Serum samples were collected on 0 and 4-dpi to measure porcine proinflammatory cytokines. Fecal scores were measured daily over the challenge period. Data from the five experiments were compiled for meta-analysis using the MIXED procedure of SAS. The NC pigs had a greater ADG (0.09 vs. -0.01 kg/d, P = 0.002), ADFI (0.24 vs. 0.21 kg/d, P = 0.09), and final BW (6.8 vs. 6.5 kg, P < 0.05). Diarrhea frequency was significantly higher in CC pigs compared with pigs on CP and NC treatments (28.5 vs. 18.7 vs. 5.3%, P < 0.05). Results from the five experiments suggest that NutriQuest Protect™ improves growth performance and reduces inflammation and diarrhea in weaned pigs artificially challenged with E. coli K88 or F18.


2008 ◽  
Vol 88 (3) ◽  
pp. 485-488 ◽  
Author(s):  
E. Kiarie ◽  
D. O. Krause ◽  
C. M. Nyachoti

Intestinal segments (10 per piglet) prepared in four anesthetized piglets were used to evaluate the effects of anti-diarrhea agents on net fluid and electrolyte losses and prostaglandin E2 (PGE2) concentrations upon infection with enterotoxigenic Escherichia coli (ETEC). Pairs of segments (non-infected and ETEC-infected) were perfused with either saline, fumaric acid (FA), zinc oxide (ZnO), egg yolk antibodies against K88 fimbriae (EYA) or carbadox (AB) during a 7.5-h period. Segments perfused with saline had higher (P < 0.05) net fluid and electrolyte losses compared to segments perfused with anti-diarrhea agents whilst FA showed higher fluid losses compared to other anti-diarrhea agents. Key words: Anti-diarrhea agents, enterotoxigenic Escherichia coli, piglets


2016 ◽  
Vol 94 (suppl_3) ◽  
pp. 395-398 ◽  
Author(s):  
M. A. Bouwhuis ◽  
T. Sweeney ◽  
M. J. McDonnell ◽  
D. N. Doyle ◽  
K. Thornton ◽  
...  

animal ◽  
2011 ◽  
Vol 5 (8) ◽  
pp. 1170-1178 ◽  
Author(s):  
R.D. Slade ◽  
I. Kyriazakis ◽  
S.M. Carroll ◽  
F.H. Reynolds ◽  
I.J. Wellock ◽  
...  

Toxins ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 760
Author(s):  
Shahnawaz Butt ◽  
Mazen Saleh ◽  
Jeffrey Gagnon

Enterotoxigenic Escherichia coli (ETEC) produces the heat-stable enterotoxin b (STb), which is responsible for secretory diarrhea in humans and animals. This toxin is secreted within the intestinal lumen of animals and humans following ETEC colonization, becoming active on enterocytes and altering fluid homeostasis. Several studies have outlined the nature of this toxin and its effects on gut health and the integrity of the intestinal epithelium. This review summarizes the mechanisms of how STb alters the gastrointestinal tract. These include the manipulation of mucosal tight junction protein integrity, the formation of enterocyte cellular pores and toxin internalization and the stimulation of programmed cell death. We conclude with insights into the potential link between STb intoxication and altered gut hormone regulation, and downstream physiology.


2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Hongbo Yi ◽  
Li Wang ◽  
Yunxia Xiong ◽  
Zhilin Wang ◽  
Yueqin Qiu ◽  
...  

Intestinal epithelial barrier damage disrupts immune homeostasis and leads to many intestinal disorders. Lactobacillus reuteri strains have probiotic functions in their modulation of the microbiota and immune system in intestines. In this study, the effects of L. reuteri LR1, a new strain isolated from the feces of weaning piglets, on intestinal epithelial barrier damage in IPEC-1 cells caused by challenge with enterotoxigenic Escherichia coli (ETEC) K88 were examined. It was found that L. reuteri LR1, in large part, offset the ETEC K88-induced increase in permeability of IPEC-1 cell monolayers and decreased the adhesion and invasion of the coliform in IPEC-1 cells. In addition, L. reuteri LR1 increased transcript abundance and protein contents of tight junction (TJ) proteins zonula occluden-1 (ZO-1) and occludin in ETEC K88-infected IPEC-1 cells, whereas it had no effects on claudin-1 and F-actin expression. Using colloidal gold immunoelectron microscopy, these effects of L. reuteri LR1 on ZO-1 and occludin content in IPEC-1 cells were confirmed. By using ML-7, a selective inhibitor of myosin light-chain kinase (MLCK), the beneficial effect of L. reuteri LR1 on contents of ZO-1 and occludin was shown to be dependent on the MLCK pathway. In conclusion, L. reuteri LR1 had beneficial effects on epithelial barrier function consistent with increasing ZO-1 and occludin expression via a MLCK-dependent manner in IPEC-1 cells during challenge with ETEC K88.


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