scholarly journals Host cell responses to Listeria monocytogenes infection include differential transcription of host stress genes involved in signal transduction.

1994 ◽  
Vol 91 (14) ◽  
pp. 6428-6432 ◽  
Author(s):  
W. R. Schwan ◽  
W. Goebel
1999 ◽  
Vol 372 (1) ◽  
pp. 166-172 ◽  
Author(s):  
Michael Kuhn ◽  
Thilo Pfeuffer ◽  
Lars Greiffenberg ◽  
Werner Goebel

2006 ◽  
Vol 74 (3) ◽  
pp. 1528-1536 ◽  
Author(s):  
Brandon B. Porter ◽  
John T. Harty

ABSTRACT The CD8+-T-cell response to infection with Listeria monocytogenes consists of expansion, contraction, and memory phases. The transition between expansion and contraction is reported to occur on different days postinfection with virulent (8 to 9 days) and attenuated (ΔactA) (7 days) L. monocytogenes strains. We hypothesized that differences in the infectious courses, and therefore antigen (Ag) display, determine the precise time of the expansion/contraction transition in response to these infections. To test this, we infected BALB/c mice with 0.1 50% lethal dose of ΔactA or virulent L. monocytogenes and measured bacterial numbers, Ag display, and Ag-specific CD8+-T-cell responses on various days after infection. We found that bacterial numbers and Ag display peaked between 12 and 36 h and between 36 and 60 h after infection with ΔactA and virulent L. monocytogenes strains, respectively. Infection with ΔactA L. monocytogenes resulted in a sharp peak in the Ag-specific CD8+-T-cell response on day 7, while infection with virulent L. monocytogenes yielded a prolonged peak with equivalent numbers of Ag-specific CD8+ T cells on days 6, 7, and 8 after infection. Truncating virulent infection with antibiotics on day 1 or 2 after infection resulted in a shift in the expansion/contraction transition from day 8 to day 7 after infection. However, antibiotic treatment beginning on day 3, after the peak of virulent L. monocytogenes infection and Ag display, had no effect upon the magnitude or timing of the CD8+-T-cell response. These results demonstrate a direct relationship between the course of infection and Ag display and that the timing of these events is important in shaping the T-cell response to infection.


2005 ◽  
Vol 201 (9) ◽  
pp. 1447-1457 ◽  
Author(s):  
Mischo Kursar ◽  
Uta E. Höpken ◽  
Markus Koch ◽  
Anne Köhler ◽  
Martin Lipp ◽  
...  

Effective priming of T cell responses depends on cognate interactions between naive T cells and professional antigen-presenting cells (APCs). This contact is the result of highly coordinated migration processes, in which the chemokine receptor CCR7 and its ligands, CCL19 and CCL21, play a central role. We used the murine Listeria monocytogenes infection model to characterize the role of the CCR7/CCR7 ligand system in the generation of T cell responses during bacterial infection. We demonstrate that efficient priming of naive major histocompatibility complex (MHC) class Ia–restricted CD8+ T cells requires CCR7. In contrast, MHC class Ib–restricted CD8+ T cells and MHC class II–restricted CD4+ T cells seem to be less dependent on CCR7; memory T cell responses are independent of CCR7. Infection experiments with bone marrow chimeras or mice reconstituted with purified T cell populations indicate that CCR7 has to be expressed on CD8+ T cells and professional APCs to promote efficient MHC class Ia–restricted T cell priming. Thus, different T cell subtypes and maturation stages have discrete requirements for CCR7.


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