Registration for a live webinar on 'Neuroleptic malignant syndrome' is now open.
See webinar detailsWe noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- Outline
- Salmonellae: ubiquitous pathogens
- Human diseases associated with Salmonellae
- Species specificity and disease
- Gastrointestinal infections
- Risk factors: gastrointestinal infections
- Bacterial foodborne diseases in the US
- Salmonellosis outbreaks linked to alfalfa sprouts
- Recent Salmonella outbreaks
- Salmonella St. Paul outbreak 2008
- Salmonella pathogenesis
- Salmonella colonize Peyer's patches
- How does Salmonella manipulate host cells?
- Type III secretion system (TTSS)
- Needle complex assembly pathway
- Salmonella encode two TTSS
- SPI1 and SPI2 translocation
- SPI1 mediates enteropathogenesis
- Salmonella enter cells by macropinocytosis
- SPI-1 effectors modify actin structure
- Small GTPase activation
- SPI induced effectors
- Inflammation is induced by signaling
- TLR's and NLR's induced inflammation
- How does Salmonella survive in the phagosome?
- How bacteria resist innate immunity and replicate
- The PhoP/PhoQ system is required for virulence
- The PhoPQ two-component system
- PhoP/PhoQ system is induced in phagosomes
- The PhoP/PhoQ signals
- Structural classes of antimicrobial peptides
- PhoQ has a PAS domain, not a binding pocket
- PhoQ has a PAS Domain with novel alpha helices
- Ca++ bound state of the PhoQ sensor domain
- Metal mediates PhoQ contact with the membrane
- Antimicrobial peptide and metal binding sites
- A model for signaling
- Sensing acidic pH by a different mechanism
- pH affects the conformation of the PhoQ sensor
- H157R mutation stabilizes low pH conformation
- Rigidity in acidic patch promotes repressed state
- Network destabilization increased helix movement
- The PhoQ periplasmic domain
- Remodel bacterial surface
- Bacterial envelope remodeling
- PhoPQ represses synthesis of organelles
- Antimicrobial peptide resistance genes
- Salmonella typhimurium LPS modifications
- Modifications associated with peptide resistance
- Bacterial resistance mechanisms to peptides
- Modify host processes
- SPI1 and SPI2 TTSS are expressed temporally
- Phagosome localization and morphological change
- Salmonellae phagosome tubulation
- Possible functions of phagosome tubulation
- What are phagosome tubulations?
- What is the role of SifA?
- A family that activates small GTPase pathways
- SifA-SKIP complex demonstrates two domains
- The SifA-SKIP complex showing the WxxE motif
- SifA-C terminus: similar to Salmonella GEF SopE
- SifA alone does not induce endosomal tubulation
- SifA and SseJ induce endosomal tubulation
- SseJ is similar to mammalian GCAT proteins
- SseJ enzymatic activity is required for tubulation
- Is RhoA the SifA target?
- RhoA induces SseJ-coated membranes extension
- Other GTPases do not induce tubulation with SseJ
- SseJ binds RhoA
- SifA binds to GDP-bound RhoA
- A possible complex SKIP/SifA/RhoA/GDP SseJ
- Salmonella induced phagosome tubulation model
- Summary
Topics Covered
- Salmonellae
- Gram-negative bacteria that cause gastroenteritis and systemic disease or enteric fever
- Mechanisms of bacterial pathogenesis include: sensing host environments through a specific receptor, remodeling the bacterial surface, and altering host cells processes
- A receptor that recognizes antimicrobial peptides and low pH
- Regulation of the structure of lipopolysaccharide, and alteration of the Salmonella-containing phagosome by use of a specialized secretion system that functions to accomplish protein transport to the mammalian cell cytoplasm
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Miller, S. (2009, October 29). Salmonellae: molecular basis of infection [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 11, 2024, from https://doi.org/10.69645/KSRE9463.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Samuel Miller has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.