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1. Introduction
2. Host-pathogen interactions
3. Successive steps of human listeriosis
4. Listeriosis as a model of infection
5. Towards understanding of human listeriosis
6. L. monocytogenes discovered by Murray in 1926
7. Listeria: the rise of a multifaceted model
8. Entry into non phagocytic cells
9. Successive steps of cell infectious process
10. Cell infectious process: bacterial factors
11. The L. monocytogenes virulence gene regulon
12. The 5' UTR can adopt a secondary structure
13. Thermoregulation of virulence genes
14. The prfA-UTR can function as a thermosensor
15. Take home messages (1)
16. The actin comet-like tails of Listeria (1)
17. The actin comet-like tails of Listeria (2)
18. The actin-based motility of Listeria
19. ActA is responsible for actin based motility
20. Arp2/3 - mediated actin assembly
21. Listeria is not the only bacterium able to move (1)
22. Arp2/3 - mediated motility in Shigella flexneri
23. Two types of comet tails
24. Listeria is not the only bacterium able to move (2)
25. Take home messages (2)
26. Bacterial-induced phagocytosis (1)
27. Bacterial-induced phagocytosis (2)
28. The inlAB operon
29. Internalin (InlA)
30. E-cadherin homophilic interactions
31. Interaction between internalin and E-cadherin (1)
32. Role of intra-cytoplasmic domain of E-cadherin
33. Arp2/3 recruited at InlA-dependent entry site
34. Cortactin, Arp2/3 and actin colocalize at entry
35. Recruitment at site of entry summary (1)
36. Two-hybrid screen using a-catenin: ARHGAP10
37. ARHGAP10 recruited at Listeria entry site
38. ARHGAP10 siRNA inhibits a-catenin recruitment
39. Recruitment at site of entry summary (2)
40. Take home messages (3)
41. Interaction between internalin and E-cadherin (2)
42. Species-specificity
43. Transgenic mice that express human E-cadherin
44. Internalin-dependent crossing of intestinal barrier
45. Take home messages (4)
46. Structure of the internalin-E-cadherin co-crystal
47. Pending questions
48. InlB, the second invasion protein (1)
49. InlB, the second invasion protein (2)
50. The InlB signaling pathway
51. Endocytosis and degradation of RTKs
52. What is clathrin mediated endocytosis?
53. Questions
54. Listeria and InlB promote ubiquitination of Met
55. InlB induces the ubiquitination, endocytosis of Met
56. The endocytosis machinery is involved in entry
57. Listeria, clathrin and dynamin at entry sites
58. Listeria exploits endocytosis machinery to enter
59. Model: exploitation of the endocytosis machinery
60. Take home messages (5)
61. Non classical clathrin recruitment around Listeria
62. Actin polymerisation follows clathrin recruitment
63. Take home messages (6)
64. A rule rather than an exception?
65. Zipper mechanism and trigger mechanism
66. E. coli, S. aureus and L. innocua recruit clathrin
67. Triggering bacteria do not use clathrin
68. Clathrin - conclusions
69. Summary of InlA and lnlB pathways
70. What is the role of InlB in vivo?
71. Species specificity of InlB
72. No role for InlB in crossing the intestinal barrier
73. Take home messages (7)
74. InlA and InlB interdependent roles
75. Some Listeria express a truncated internalin
76. Epidemiological survey on 450 strains
77. Anatomy of the human placental barrier
78. Study of placenta from patients with listeriosis
79. A role for internalin in crossing placental barrier?
80. Crossing the placental barrier in-vivo/ex-vivo
81. Search for a small animal model
82. Entry in gerbil depends on both inlA and inlB
83. In vivo imaging of listeriosis in gerbils
84. Interdependent roles of InlA, InlB in infection
85. Knock-in mice expressing human E16P mEcad
86. InlA and InlB - conclusions
87. Take home messages (8)
88. Comparative genomics
89. The bsh gene is absent from Listeria innocua
90. BSH is critical for persistence in intestinal tract
91. L. monocytogenes and histone modifications
92. Chromatin and nucleosome structure
93. Histone modifications and transcriptional regulation
94. Listeria decreases phosphorylated H3
95. Listeria induces specific histone modifications
96. LLO induces dephosphorylation of H3
97. LLO histone modifications prior to cell invasion
98. LLO pathway remains unknown
99. LLO induces a specific transcriptional response
100. LLO transcription changes and modified histone
101. LLO - conclusions
102. Perspectives/ future work
103. Epigenetics and bacterial infectious diseases
104. Contribution of the Listeria model to biology
105. Acknowledgments
106. Listeria in the cell - image

Topics Covered

• Host-pathogen interactions
• Successive steps of human listeriosis
• Listeriosis: a model of infection
• Listeria monocytogenes : the rise of a multifaceted model
• Entry into non-phagocytic cells
• The cell infection process
• The Listeria monocytogenes virulence gene regulon
• Bacterial-induced phagocytosis
• The inlAB operon
• Internalin
• E-cadherin
• ARHGAP10
• Interaction between Internalin and E-cadherin
• The InlB signaling pathway
• Endocytosis and degradation of RTKs
• Model: exploitation of the endocytosis machinery for invasion of mammalian cells
• Clathrin
• Is the mechanism used by Listeria a rule rather than an exception?
• What is the role of InlB in vivo?
• Epidemiological survey
• InlA and InlB play interdependent roles during feto-placental listeriosis
• Roles of InlA and InlB in infection
• Comparative genomics
• Histone modifications
• Epigenetics and bacterial infectious diseases
• Contribution of the Listeria model to biology

Links

Series:

• Molecular Basis of Bacterial Infection

Categories:

• Clinical Practice
• Microbiology

Therapeutic Areas:

• Infectious Diseases

Talk Citation

Cossart, P. (2009, December 7). The bacterial pathogen Listeria monocytogenes: an amazing multifaceted model [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved April 15, 2025, from https://doi.org/10.69645/LZOA5469.
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Publication History

• Published on December 7, 2009

Financial Disclosures

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