scholarly journals Establishment and application of isothermal amplification techniques for the detection of heat-stable I enterotoxin of enterotoxigenic Escherichia coli

PLoS ONE ◽  
2020 ◽  
Vol 15 (4) ◽  
pp. e0230881
Author(s):  
Junjun Zhai ◽  
Zhang Yan ◽  
Feng Ping ◽  
Qu Lei ◽  
Xuelong Chen ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Isothermal Amplification ◽  
Enterotoxigenic Escherichia Coli ◽  
Heat Stable

Use of a Multiplex PCR System for the Simultaneous Detection of Heat Labile Toxin I and Heat Stable Toxin II Genes of Enterotoxigenic Escherichia coli in Skim Milk and Porcine Stool

1998 ◽  
Vol 61 (2) ◽  
pp. 141-145 ◽  
Author(s):  
HAU-YANG TSEN ◽  
LIANG-ZHAO JIAN ◽  
WAN-RONG CHI
Keyword(s):  
Escherichia Coli ◽  
Multiplex Pcr ◽  
Simultaneous Detection ◽  
Skim Milk ◽  
Pcr Primers ◽  
Enterotoxigenic Escherichia Coli ◽  
Farm Animals ◽  
Target Cells ◽  
Heat Stable ◽  
Heat Labile

Enterotoxigenic Escherichia coli (ETEC) strains which produce heat labile and/or heat stable toxins (LT and ST) may cause diarrhea in humans and farm animals. Using PCR primers specific for the LT I and ST II genes, a multiplex PCR system which allows detection of LT I- and ST II-producing ETEC strains was developed. When skim milk was used for a PCR assay, it was found that if target cells in the sample were precultured in MacConkey broth for 8 h prior to PCR as few as 100 cells per ml of the sample could be detected. Without the preculture step, 104 CFU of target cells per 0.2 g of porcine stool specimen were required to generate visible PCR products. The multiplex PCR System can be used for rapid testing of fecal specimens, food and possibly environmental samples for the presence of ETEC strains.

Synthesis and biological properties of carba-analogs of heat-stable enterotoxin (ST) produced by enterotoxigenic Escherichia coli

1991 ◽  
Vol 176 (3) ◽  
pp. 958-965 ◽  
Author(s):  
Yuji Hidaka ◽  
Katsuhiko Ohmori ◽  
Akihiro Wada ◽  
Hiroshi Ozaki ◽  
Hideaki Ito ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Biological Properties ◽  
Enterotoxigenic Escherichia Coli ◽  
Heat Stable

scholarly journals Chemical properties of heat-stable enterotoxins produced by enterotoxigenic Escherichia coli of different host origins.

1983 ◽  
Vol 42 (2) ◽  
pp. 539-548 ◽  
Author(s):  
L A Dreyfus ◽  
J C Frantz ◽  
D C Robertson
Keyword(s):  
Escherichia Coli ◽  
Chemical Properties ◽  
Enterotoxigenic Escherichia Coli ◽  
Heat Stable

Inhibition of Escherichia coli heat-stable enterotoxin by indomethacin and chlorpromazine

1980 ◽  
Vol 29 (3) ◽  
pp. 908-913
Author(s):  
R N Greenberg ◽  
F Murad ◽  
B Chang ◽  
D C Robertson ◽  
R L Guerrant
Keyword(s):  
Escherichia Coli ◽  
Guanylate Cyclase ◽  
Fluid Secretion ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Enterotoxigenic Escherichia Coli ◽  
Fluid Accumulation ◽  
Intestinal Tissue ◽  
Suckling Mice ◽  
Heat Stable

Purified heat-stable enterotoxin (ST) from a procine strain of enterotoxigenic Escherichia coli activates quanylate cyclase in particulate fractions of rat intestinal tissue and induces fluid accumulation in suckling mice. These effects of ST were examined in the presence of either indomethacin or chlorpromazine. We also examined the effects of these two drugs on fluid accumulation in suckling mice induced by the 8-bromo analog of cyclic guanosine monophosphate. Either indomethacin or chlorpromazine reduced ST activation of guanylate cyclase. Both drugs also reduced intestinal fluid accumulation in suckling mice that resulted from submaximal doses of ST (both P < 0.001). However, there was no reduction in fluid secretion by either drug when a maximally effective dose of ST was used, suggesting that inhibition of fluid secretion by both drugs can be overcome by increasing the ST dose and that a threshold level of guanylate cyclase activity results in maximal secretory response. Both drugs also reduced basal guanylate cylase activity in rat intestinal tissue and fluid secreton in suckling mice. Chlorpromazine also reduced intestinal secretion mediated by 8-bromo cyclic guanosine monophosphate (P < 0.001). These findings indicate that chlorpromazine interferes with the effects of ST both before and after its activation of guanylate cyclase, whereas indomethacin interfers with ST only before its activation of guanylate cyclase.

Crystallization and X-ray analysis of the toxic domain of heat-stable enterotoxin of enterotoxigenic Escherichia coli

Peptides ◽  
1992 ◽  
pp. 295-296
Author(s):  
Takashi Sato ◽  
Hiroshi Ozaki ◽  
Yasuo Hata ◽  
Yukiteru Katsube ◽  
Yasutsugu Shimonishi
Keyword(s):  
Escherichia Coli ◽  
Enterotoxigenic Escherichia Coli ◽  
X Ray ◽  
Heat Stable

scholarly journals Clinical aspects of heat-labile and heat-stable toxin-producing enterotoxigenic Escherichia coli: A prospective study among Finnish travellers

2020 ◽  
Vol 38 ◽  
pp. 101855
Author(s):  
Katri Turunen ◽  
Jenni Antikainen ◽  
Tinja Lääveri ◽  
Juha Kirveskari ◽  
Ann-Mari Svennerholm ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Prospective Study ◽  
Enterotoxigenic Escherichia Coli ◽  
Clinical Aspects ◽  
Heat Stable ◽  
Heat Labile ◽  
A Prospective Study

scholarly journals Enterotoxigenic Escherichia coli Prevents Host NF-κB Activation by Targeting IκBα Polyubiquitination

2012 ◽  
Vol 80 (12) ◽  
pp. 4417-4425 ◽  
Author(s):  
Xiaogang Wang ◽  
Philip R. Hardwidge
Keyword(s):  
Escherichia Coli ◽  
Immune Responses ◽  
Diarrheal Disease ◽  
Innate Immune ◽  
Host Cells ◽  
Enterotoxigenic Escherichia Coli ◽  
Host Responses ◽  
Innate Immune Responses ◽  
Content Type ◽  
Heat Stable

ABSTRACTThe NF-κB pathway regulates innate immune responses to infection. NF-κB is activated after pathogen-associated molecular patterns are detected, leading to the induction of proinflammatory host responses. As a countermeasure, bacterial pathogens have evolved mechanisms to subvert NF-κB signaling. EnterotoxigenicEscherichia coli(ETEC) causes diarrheal disease and significant morbidity and mortality for humans in developing nations. The extent to which this important pathogen subverts innate immune responses by directly targeting the NF-κB pathway is an understudied topic. Here we report that ETEC secretes a heat-stable, proteinaceous factor that blocks NF-κB signaling normally induced by tumor necrosis factor (TNF), interleukin-1β, and flagellin. Pretreating intestinal epithelial cells with ETEC supernatant significantly blocked the degradation of the NF-κB inhibitor IκBα without affecting IκBα phosphorylation. Data from immunoprecipitation experiments suggest that the ETEC factor functions by preventing IκBα polyubiquitination. Inhibiting clathrin function blocked the activity of the secreted ETEC factor, suggesting that this yet-uncharacterized activity may utilize clathrin-dependent endocytosis to enter host cells. These data suggest that ETEC evades the host innate immune response by directly modulating NF-κB signaling.

Repression of heat-stable enterotoxin synthesis in enterotoxigenic Escherichia coli.

1977 ◽  
Vol 17 (3) ◽  
pp. 629-633 ◽  
Author(s):  
J F Alderete ◽  
D C Robertson
Keyword(s):  
Escherichia Coli ◽  
Enterotoxigenic Escherichia Coli ◽  
Heat Stable
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