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- Principles in Bacterial Pathogenesis
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1. The molecular basis of bacterial pathogenicity: an overview
- Prof. B. Brett Finlay
- Gram Negative Pathogens
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2. Deciphering shigella invasion of epithelial cells
- Prof. Philippe Sansonetti
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5. Bordetella pertussis
- Prof. Alison Weiss
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6. Salmonellae: molecular basis of infection
- Prof. Samuel Miller
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7. The diversity of Escherichia coli infections
- Prof. Michael Donnenberg
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8. Bacterial activation of epithelial signaling
- Prof. Alice Prince
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9. Human pathogenic Yersinia species
- Prof. James Bliska
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11. Dental pathogens
- Prof. Ann Progulske-Fox
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12. Haemophilus
- Prof. Robert Munson
- Gram Positive Pathogens
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13. The bacterial pathogen Listeria monocytogenes: an amazing multifaceted model
- Prof. Pascale Cossart
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15. Molecular pathogenesis and prevention of Staphylococcus aureus infections
- Prof. Olaf Schneewind
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16. Streptococcus pyogenes disease and molecular pathogenesis
- Prof. P. Patrick Cleary
- Host Responses
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17. Microbial recognition and the immune response
- Dr. Dana Philpott
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18. Enteric pathogens-microbiota-host inter-kingdom chemical interactions
- Prof. Vanessa Sperandio
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19. Toll-like receptor signalling during infection and inflammation
- Prof. Luke O'Neill
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20. The human indigenous microbiota
- Prof. David Relman
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22. Role of neutrophils in acute lung injury and repair
- Prof. Gregory Downey
- Preventatives and Therapeutics
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23. Antibiotics and antibiotic resistance
- Prof. Gerry Wright
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24. Vaccines: a health insurance of the 21st century
- Prof. Rino Rappuoli
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25. Biodefense vaccines
- Prof. James Nataro
- Archived Lectures *These may not cover the latest advances in the field
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26. Vaccines in the modern world
- Prof. Gordon Dougan
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27. Bacterial infection of epithelial signaling
- Prof. Alice Prince
Printable Handouts
Navigable Slide Index
- Introduction
- Talk outline
- Bacterial adaptation
- Pathogens in CF
- Overview
- P. aeruginosa adaptations
- CFTR-PTEN complex
- CFTR and PTEN in real people
- PTEN insufficiency in CF cells
- P. aeruginosa changes in CF
- P. aeruginosa and succinate
- Long term bacterial mutations
- Changes due to mutation
- Host-pathogen interaction
- Host-adapted strains in mice
- Metabolic changes over time
- Conditions in the CF lung
- Conclusion
Topics Covered
- Bacterial interactions with epithelium
- Cystic fibrosis (CF) model
- Pathogens in CF
- Pseudomonas aeruginosa adaptations
- CFTR and PTEN dysfunction
- Long term bacterial mutations
- Host-pathogen interactions
- Pseudomonas aeruginosa in CF
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Prince, A. (2021, August 30). Bacterial activation of epithelial signaling [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 1, 2024, from https://doi.org/10.69645/IUQA2410.Export Citation (RIS)
Publication History
Financial Disclosures
- There are no financial matters to disclose.
A selection of talks on Microbiology
Transcript
Please wait while the transcript is being prepared...
0:00
This is an update of a talk about bacterial activation of epithelial signalling.
In the earlier material I reviewed how bacterial components stimulate
the airway epithelium, to activate inflammation, and to
start the clearance of infection in the human lung and the airway.
0:19
In the next few slides, I'd like to go over some newer information
as to how bacteria interact with the epithelium,
particularly how they activate immunometabolites, and how this is important in infection.
We're going to use cystic fibrosis as a model, because this is
a very well-known disease that affects airway epithelial cells as well as immune cells.
There's an abnormal chloride channel that affects the milieu of the human airway.
We want to know how this epithelial signaling and how these changes in
epithelial metabolism impact upon the pathogenesis of infection.
1:01
How do bacteria adapt to the airway epithelium?
They're inhaled and they can adapt due to immune pressure,
the macrophages that try to remove them,
we know from looking at colonies of bacteria from the lungs, we often see small colony variants,
where we see grossly mucoid strains that we only see in this one situation.
The other question is: is it metabolic pressure that is causing
these organisms to change their surface characteristics?
It's felt that these surface components make the organisms more resistant to phagocytosis,
but they could also be protecting the organisms from other things, like oxidative stress.
Again, cystic fibrosis is a great model because it's very well known that cystic fibrosis
isolates of organisms such as Pseudomonas aeruginosa are often mucoid,
or we see these small colony variants, so they have adapted to their long-term residence in the lung.