The effect of maternal and postweaning seaweed extract supplementation on gut health in pigs after weaning and response to enterotoxigenic Escherichia coli K88 challenge1

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


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.


2008 ◽  
Vol 99 (3) ◽  
pp. 520-530 ◽  
Author(s):  
I. J. Wellock ◽  
P. D. Fortomaris ◽  
J. G. M. Houdijk ◽  
J. Wiseman ◽  
I. Kyriazakis

The inclusion of insoluble NSP (iNSP) in weaner pig diets has been reported to decrease post-weaning colibacillosis (PWC). Conversely, soluble NSP (sNSP) have been shown to exacerbate PWC. The present study investigated the effect of NSP solubility and inclusion level on the health and performance of newly weaned pigs challenged with enterotoxigenic Escherichia coli (ETEC), using NSP sources known not to affect digesta viscosity, in a 2 ×  2 ×  2 factorial combination of NSP solubility (iNSP v. sNSP), inclusion level (low (L; 50 g/kg) v. high (H; 150 g/kg)) and ETEC challenge (infected v. sham). Infection had no effect on pig health, but reduced performance to a larger extent in pigs on the L diets compared with those on the H diets. The inclusion of sNSP significantly decreased the occurrence of diarrhoea (P < 0·001) and improved gut health, as indicated by a lower caecal digesta pH (P = 0·008) and increased (P = 0·002) Lactobacillus:coliform ratio, when compared with the iNSP diet on day 14 post-weaning. There was no effect of NSP solubility on ETEC shedding, digesta viscosity or pig performance. Pigs on the H diets had fewer cases of diarrhoea and shed fewer ETEC than those on the L diets. Increasing NSP inclusion significantly increased colonic Lactobacillus:coliform ratio, volatile fatty acid concentration and caecal digesta viscosity, but decreased performance. These results suggest that sNSP per se are not detrimental to pig health and that increasing the concentration of NSP in weaner diets that do not increase digesta viscosity may have a beneficial effect on gut health and protect against PWC.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Charles R. Midgett ◽  
Kacey Marie Talbot ◽  
Jessica L. Day ◽  
George P. Munson ◽  
F. Jon Kull

AbstractEnteric infections caused by the gram-negative bacteria enterotoxigenic Escherichia coli (ETEC), Vibrio cholerae, Shigella flexneri, and Salmonella enterica are among the most common and affect billions of people each year. These bacteria control expression of virulence factors using a network of transcriptional regulators, some of which are modulated by small molecules as has been shown for ToxT, an AraC family member from V. cholerae. In ETEC the expression of many types of adhesive pili is dependent upon the AraC family member Rns. We present here the 3 Å crystal structure of Rns and show it closely resembles ToxT. Rns crystallized as a dimer via an interface similar to that observed in other dimeric AraC’s. Furthermore, the structure of Rns revealed the presence of a ligand, decanoic acid, that inhibits its activity in a manner similar to the fatty acid mediated inhibition observed for ToxT and the S. enterica homologue HilD. Together, these results support our hypothesis that fatty acids regulate virulence controlling AraC family members in a common manner across a number of enteric pathogens. Furthermore, for the first time this work identifies a small molecule capable of inhibiting the ETEC Rns regulon, providing a basis for development of therapeutics against this deadly human pathogen.


AMB Express ◽  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Pengpeng Xia ◽  
Yunping Wu ◽  
Siqi Lian ◽  
Guomei Quan ◽  
Yiting Wang ◽  
...  

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.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Mandi Liu ◽  
Yue Zhang ◽  
Di Zhang ◽  
Yun Bai ◽  
Guomei Liu ◽  
...  

AbstractEnterotoxigenic Escherichia coli (ETEC), an essential cause of post-weaning diarrhea (PWD) in piglets, leads to significant economic losses to the pig industry. The present study aims to identify the role of ETEC total RNA in eliciting immune responses to protect animals against ETEC infection. The results showed that the total RNA isolated from pig-derived ETEC K88ac strain effectively stimulated the IL-1β secretion of porcine intestinal epithelial cells (IPEC-J2). The mouse model immunized with ETEC total RNA via intramuscular injection (IM) or oral route (OR) was used to evaluate the protective efficiency of the ETEC total RNA. The results suggested that 70 μg ETEC total RNA administered by either route significantly promoted the production of the serum IL-1β and K88ac specific immunoglobulins (IgG, IgM, and IgA). Besides, the ETEC RNA administration augmented strong mucosal immunity by elevating K88ac specific IgA level in the intestinal fluid. Intramuscularly administered RNA induced a Th1/Th2 shift toward a Th2 response, while the orally administered RNA did not. The ETEC total RNA efficiently protected the animals against the ETEC challenge either by itself or as an adjuvant. The histology characterization of the small intestines also suggested the ETEC RNA administration protected the small intestinal structure against the ETEC infection. Particularly of note was that the immunity level and protective efficacy caused by ETEC RNA were dose-dependent. These findings will help understand the role of bacterial RNA in eliciting immune responses, and benefit the development of RNA-based vaccines or adjuvants.


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