Host-specific fimbrial adhesins of noninvasive enterotoxigenic Escherichia coli strains.

1982 ◽  
Vol 46 (2) ◽  
pp. 129-161 ◽  
Author(s):  
W Gaastra ◽  
F K de Graaf
Biology ◽  
2013 ◽  
Vol 2 (3) ◽  
pp. 894-917 ◽  
Author(s):  
Emanuela Lonardi ◽  
Kristof Moonens ◽  
Lieven Buts ◽  
Arjen de Boer ◽  
Johan Olsson ◽  
...  

2016 ◽  
Vol 46 (8) ◽  
pp. 1430-1437 ◽  
Author(s):  
Daniele Araujo Pereira ◽  
Marilda Carlos Vidotto ◽  
Karla Alvarenga Nascimento ◽  
Anne Caroline Ramos dos Santos ◽  
Marina Lopes Mechler ◽  
...  

ABSTRACT: Enterotoxigenic Escherichia coli (ETEC) is the major cause of diarrhea in newborn and weaned pigs. Bacteria adhesion to the host cell is considered a specific phenomenon among fimbrial and non-fimbrial adhesins with their respective receptors on enterocytes. Enteric disorders are related with the fimbriae F4 (K88), F5 (K99), F6 (987P), F41, and F18. In addition to ETEC, another category of E. coli , porcine pathogenic E. coli (PEPEC),can cause diarrhea in pigs; it produces the porcine attaching and effacing-associated (Paa) adhesin in, which is capable to cause a typical lesion known as an attaching and effacing (A/E) lesion. Immunization of sows with adhesin is important to stimulate the production of antibodies and their subsequent transfer to piglets through colostrum. The aim of this paper is to illustrate the main impacts of enteric diseases caused by E. coli in swine production and to highlight the importance of continuing research on this bacterium to improve disease prevention through vaccination.


1992 ◽  
Vol 29 (3) ◽  
pp. 239-246 ◽  
Author(s):  
B. Nagy ◽  
L. H. Arp ◽  
H. W. Moon ◽  
T. A. Casey

Intestinal colonization of 3-week-old weaned pigs by enterotoxigenic Escherichia coli (ETEC) strains that were originally isolated from weaned pigs with fatal diarrhea and that lacked K88, K99, F41, and 987P adhesins (4P− ETEC) was studied by histologic, immunofluorescent, and electron microscopic techniques. In the first experiment, 16 principal pigs were inoculated orogastrically with ETEC strain 2134 (serogroup 0157:H19) or 2171 (serogroup 0141:H4), and eight control pigs were not inoculated. In the second experiment, 24 principals were inoculated with ETEC strain 2134, and 12 controls were inoculated with a nonenterotoxigenic strain of E. coli. Principal and control pigs were necropsied at intervals from 24 to 72 hours after inoculation of principals to provide the tissues used for this report. Results from the two experiments and with both ETEC strains were similar and therefore were combined. Adhesion by 4P″ ETEC was demonstrated in ileum but not in cecum or colon in 22/40 principal pigs sampled at 24 to 72 hours after orogastric inoculation. Adherent bacteria were most apparent on the intestinal villi covering Peyer's patches. Only occasional adherent bacteria were detected in ileal sections from a few (4/20) of the control pigs. Adherence by 4P− ETEC was characterized by “patches” of bacteria closely associated with the lateral surfaces and less frequently with the tips and the bases of intact villi. In most cases, the adherent bacteria were separated from epithelial cell microvilli and other bacterial cells by a 50–400-nm space. Filamentous bacterial appendages bridged this space and formed a network among adjacent bacteria. Colonization of weaned pigs by the 4P− ETEC strains was characterized by preferential adhesion of bacteria to the villi covering Peyer's patches. The filamentous appendages observed between bacteria and microvilli are previously unrecognized fimbrial adhesins, which mediate colonization by these ETEC.


2014 ◽  
Vol 82 (9) ◽  
pp. 3657-3666 ◽  
Author(s):  
Alaullah Sheikh ◽  
Qingwei Luo ◽  
Koushik Roy ◽  
Salwa Shabaan ◽  
Pardeep Kumar ◽  
...  

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.


1985 ◽  
Vol 49 (1) ◽  
pp. 159-163 ◽  
Author(s):  
H W van Verseveld ◽  
P Bakker ◽  
T van der Woude ◽  
C Terleth ◽  
F K de Graaf

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.


Sign in / Sign up

Export Citation Format

Share Document