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1. Introduction
2. Outline
3. Salmonellae: ubiquitous pathogens
4. Human diseases associated with Salmonellae
5. Species specificity and disease
6. Gastrointestinal infections
7. Risk factors: gastrointestinal infections
8. Bacterial foodborne diseases in the US
9. Salmonellosis outbreaks linked to alfalfa sprouts
10. Recent Salmonella outbreaks
11. Salmonella St. Paul outbreak 2008
12. Salmonella pathogenesis
13. Salmonella colonize Peyer's patches
14. How does Salmonella manipulate host cells?
15. Type III secretion system (TTSS)
16. Needle complex assembly pathway
17. Salmonella encode two TTSS
18. SPI1 and SPI2 translocation
19. SPI1 mediates enteropathogenesis
20. Salmonella enter cells by macropinocytosis
21. SPI-1 effectors modify actin structure
22. Small GTPase activation
23. SPI induced effectors
24. Inflammation is induced by signaling
25. TLR's and NLR's induced inflammation
26. How does Salmonella survive in the phagosome?
27. How bacteria resist innate immunity and replicate
28. The PhoP/PhoQ system is required for virulence
29. The PhoPQ two-component system
30. PhoP/PhoQ system is induced in phagosomes
31. The PhoP/PhoQ signals
32. Structural classes of antimicrobial peptides
33. PhoQ has a PAS domain, not a binding pocket
34. PhoQ has a PAS Domain with novel alpha helices
35. Ca++ bound state of the PhoQ sensor domain
36. Metal mediates PhoQ contact with the membrane
37. Antimicrobial peptide and metal binding sites
38. A model for signaling
39. Sensing acidic pH by a different mechanism
40. pH affects the conformation of the PhoQ sensor
41. H157R mutation stabilizes low pH conformation
42. Rigidity in acidic patch promotes repressed state
43. Network destabilization increased helix movement
44. The PhoQ periplasmic domain
45. Remodel bacterial surface
46. Bacterial envelope remodeling
47. PhoPQ represses synthesis of organelles
48. Antimicrobial peptide resistance genes
49. Salmonella typhimurium LPS modifications
50. Modifications associated with peptide resistance
51. Bacterial resistance mechanisms to peptides
52. Modify host processes
53. SPI1 and SPI2 TTSS are expressed temporally
54. Phagosome localization and morphological change
55. Salmonellae phagosome tubulation
56. Possible functions of phagosome tubulation
57. What are phagosome tubulations?
58. What is the role of SifA?
59. A family that activates small GTPase pathways
60. SifA-SKIP complex demonstrates two domains
61. The SifA-SKIP complex showing the WxxE motif
62. SifA-C terminus: similar to Salmonella GEF SopE
63. SifA alone does not induce endosomal tubulation
64. SifA and SseJ induce endosomal tubulation
65. SseJ is similar to mammalian GCAT proteins
66. SseJ enzymatic activity is required for tubulation
67. Is RhoA the SifA target?
68. RhoA induces SseJ-coated membranes extension
69. Other GTPases do not induce tubulation with SseJ
70. SseJ binds RhoA
71. SifA binds to GDP-bound RhoA
72. A possible complex SKIP/SifA/RhoA/GDP SseJ
73. Salmonella induced phagosome tubulation model
74. 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:

• Molecular Basis of Bacterial Infection

Categories:

• Clinical Practice
• Microbiology

Therapeutic Areas:

• Infectious Diseases

Talk Citation

Publication History

• Published on October 29, 2009

Financial Disclosures

• Prof. Samuel Miller has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.