scholarly journals Small intestine lactobacilli growth promotion and immunomodulation in weaner pigs fed Cyberlindnera jadinii yeast high inclusion diet and exposed to enterotoxigenic Escherichia coli F4+: O149

2021 ◽  
Author(s):  
S. Iakhno ◽  
S.S. Hellestveit ◽  
Ö.C.O. Umu ◽  
L.T. Bogevik ◽  
C.P. Åkesson ◽  
...  

1AbstractEnterotoxigenic Escherichia coli (ETEC) F4+: O149 is a causative agent for the development of post-weaning diarrhoea (PWD) in pigs that contributes to production losses. Yeast cell wall components used as a feed additive can modulate gut immunity and help protect animals from enteric infections. This work investigated how a novel yeast diet with high inclusion of yeast proteins (40% of crude protein) affected the course of ETEC mediated diarrhoea in weaner piglets from a farm with or without a history of post-weaning diarrhoea. We found that immune response to F4ab ETEC infection and appetite of the animals were altered by high inclusion C. jadinii yeast. The results indicate that the novel diet can support the diseased animals either directly through the effect of yeast beta-glucans and mannans or indirectly through the promotion of small intestine lactobacilli or both.

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.


2021 ◽  
Author(s):  
Alaullah Sheikh ◽  
Tamding Wangdi ◽  
Tim J Vickers ◽  
Bailey Aaron ◽  
Margot Perrin Palmer ◽  
...  

Enterotoxigenic Escherichia coli (ETEC) are a genetically diverse pathologic variant of E. coli defined by the production of heat-labile (LT) and/or heat-stable (ST) toxins. ETEC are estimated to cause hundreds of millions of cases of diarrheal illness annually. However, it is not clear that all strains are equally equipped to cause disease and asymptomatic colonization with ETEC is common in low-middle income regions lacking basic sanitation and clean water where ETEC are ubiquitous. Recent molecular epidemiology studies have revealed a significant association between strains which produce EatA, a secreted autotransporter protein, and the development of symptomatic infection. Here, we demonstrate that LT stimulates production of MUC2 mucin by goblet cells in human small intestine, enhancing the protective barrier between pathogens and enterocytes. In contrast, using explants of human small intestine as well as small intestinal enteroids, we show that EatA counters this host defense by engaging and degrading the MUC2 mucin barrier to promote bacterial access to target enterocytes and ultimately toxin delivery suggesting that EatA plays a crucial role in the molecular pathogenesis of ETEC. These findings may inform novel approaches to prevention of the acute diarrheal illness as well as the sequelae associated with ETEC and other pathogens that rely on EatA and similar proteases for efficient interaction with their human hosts.


2006 ◽  
Vol 74 (2) ◽  
pp. 869-875 ◽  
Author(s):  
Kenneth P. Allen ◽  
Mildred M. Randolph ◽  
James M. Fleckenstein

ABSTRACT Enterotoxigenic Escherichia coli (ETEC) infections are a significant cause of diarrheal disease and infant mortality in developing countries. Studies of ETEC pathogenesis relevant to vaccine development have been greatly hampered by the lack of a suitable small-animal model of infection with human ETEC strains. Here, we demonstrate that adult immunocompetent outbred mice can be effectively colonized with the prototypical human ETEC H10407 strain (colonization factor antigen I; heat-labile and heat-stable enterotoxin positive) and that production of heat-labile holotoxin provides a significant advantage in colonization of the small intestine in this model.


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.


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