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Printable Handouts
Navigable Slide Index
- Introduction
- E. coli
- E. coli pangenome
- Enterohemorrhagic E. coli (EHEC) O157:H7
- The human pathogen E. coli O157:H7 breaches the mucosal layer to access the epithelium
- Locus of enterocyte effacement (LEE)
- Human gut is a highly populated environment: 10-100 trillions of commensal bacteria
- Bacteria sense their surroundings: two-component system (TCS)
- FusK and FusR domains
- Exploitation of microbiota released metabolites as signaling molecules by enteric pathogens (1)
- Exploitation of microbiota released metabolites as signaling molecules by enteric pathogens (2)
- Enteric pathogens exploit the microbiota
- Differential EHEC interactions with members of the GI microbiota (1)
- Differential EHEC interactions with members of the GI microbiota (2)
- Inter-kingdom chemical signaling
- Neurotransmitters affect both host and bacterial behavior, and their relationship
- Sensing epinephrine/norepinephrine
- Inter-kingdom chemical signaling integrated with gut-brain-axis
- EHEC (E. coli O157:H7) QseC regulation of virulence: intestinal infection
- EHEC vs. Citrobacter rodentium
- C. rodentium QseC regulation of virulence: intestinal infection
- Small molecule screens for QseC inhibitors
- Is all signaling stressful? Endocannabinoids in the GI tract
- The enteric endocannabinoid (EC) system
- Canonical 2-AG signaling
- Translation of inter-kingdom gut-brain-axis signaling into anti-microbial therapies
- How does manipulation of endogenous 2-AG production impact EHEC pathogenesis?
- Inhibition of 2AG biosynthesis increases pedestal formation by EHEC
- 2AG also inhibits C. rodentium virulence
- Citrobacter infection is decreased with 2AG accumulation
- Model of EC action
- Summary (1)
- Serotonin (5-HT) as a neurotransmitter
- Inter-kingdom chemical signaling integrated with gut-brain-axis
- 95% of serotonin is produced by the GI tract
- Modulation of serotonin levels in the intestine affects host susceptibility to enteric pathogens (1)
- Modulation of serotonin levels in the intestine affects host susceptibility to enteric pathogens (2)
- Modulation of serotonin levels in the intestine affects host susceptibility to enteric pathogens (3)
- Summary (3)
- QseC: a sensor for host catecholamines to regulate bacterial function in the gut
- Gut-brain axis: a two-way street in host-microbial interactions
- Drug addiction
- Effect of psychoactive drugs on pathogen virulence
- Cocaine and C. rodentium virulence
- Animal model of addiction: behavioral sensitization
- C. rodentium infection alters addiction-like behaviors
- Gut colonization by Proteobacteria modulates cocaine neurobehavioral responses
- Conclusions
- Chemical signaling in the intestine in microbe host interactions
Topics Covered
- Bacterial enteric pathogens
- Microbiota
- E. coli
- C. rodentium
- Neurotransmitters
- Epinephrine and norepinephrine
- Regulation of virulence in the gut
- Enteric endocannabinoid (EC) system
- Serotonin
- Gut-brain axis
- Cocaine neurobehavioral responses in gut colonization
Links
Series:
Categories:
Therapeutic Areas:
External Links
Talk Citation
Sperandio, V. (2024, May 30). Enteric pathogens-microbiota-host inter-kingdom chemical interactions [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 3, 2024, from https://doi.org/10.69645/NMAC7287.Export Citation (RIS)
Publication History
Financial Disclosures
- There are no commercial/financial matters to disclose.
A selection of talks on Infectious Diseases
Transcript
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0:00
Hello. Today I will
be talking about
"Enteric
Pathogens-Microbiota-Host
Inter-Kingdom Chemical
Interactions".
My name is Vanessa
Sperandio and I'm in
the Department of Medical
Microbiology and Immunology
at the University of
Wisconsin-Madison.
0:20
I will be talking about
a specific enteric
pathogen Escherichia coli.
Usually, we think about E. coli
the predominant facultative
anaerobe commensal
of the human colonic flora.
But several strains
of E. coli can also
be pathogens causing meningitis,
urinary tract infections,
and there are several
clades that cause diarrhea.
0:45
The reason E. coli is a
versatile bacteria that can be
both a commensal
and a pathogen is
because it has a
very mosaic genome.
A comparison of the genomes
of E. coli even though.
E. coli genomes vary between
4,000 and 5,000 genes,
about only 2,000 of
these genes are shared
between all of the
E. colis and the genetic
repertoire of E. coli,
which we call the
pangenome can be
as large as 13,000 genes,
and several pathogens have
extra genes in
their genomes which
are encoded in
pathogenicity islands
which allow them to
become pathogenic.
1:26
The pathogen we're
discussing today is
enterohemorrhagic E.
coli (EHEC) O157:H7.
This is a food-borne pathogen
responsible for outbreaks
of bloody diarrhea in
many countries and
these outbreaks
are important because
the younger and the
older have a high probability
of developing hemolytic
uremic syndrome
which is a complication
that leads to
high levels of morbidity
and mortality.
You get infected by
contaminated food and
water and this is a very
professional pathogen with
a very low infectious dose,
so 50 bacterial cells can
make a human being sick and
it colonizes the
large intestine.
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