scholarly journals TheLeishmania donovanichaperone cyclophilin 40 is essential for intracellular infection independent of its stage-specific phosphorylation status

2014 ◽  
Vol 93 (1) ◽  
pp. 80-97 ◽  
Author(s):  
Wai-Lok Yau ◽  
Pascale Pescher ◽  
Andrea MacDonald ◽  
Sonia Hem ◽  
Dorothea Zander ◽  
...  
2021 ◽  
Vol 9 (2) ◽  
pp. 379
Author(s):  
Breanne M. Head ◽  
Christopher I. Graham ◽  
Teassa MacMartin ◽  
Yoav Keynan ◽  
Ann Karen C. Brassinga

Legionnaires’ disease incidence is on the rise, with the majority of cases attributed to the intracellular pathogen, Legionella pneumophila. Nominally a parasite of protozoa, L. pneumophila can also infect alveolar macrophages when bacteria-laden aerosols enter the lungs of immunocompromised individuals. L. pneumophila pathogenesis has been well characterized; however, little is known about the >25 different Legionella spp. that can cause disease in humans. Here, we report for the first time a study demonstrating the intracellular infection of an L. bozemanae clinical isolate using approaches previously established for L. pneumophila investigations. Specifically, we report on the modification and use of a green fluorescent protein (GFP)-expressing plasmid as a tool to monitor the L. bozemanae presence in the Acanthamoeba castellanii protozoan infection model. As comparative controls, L. pneumophila strains were also transformed with the GFP-expressing plasmid. In vitro and in vivo growth kinetics of the Legionella parental and GFP-expressing strains were conducted followed by confocal microscopy. Results suggest that the metabolic burden imposed by GFP expression did not impact cell viability, as growth kinetics were similar between the GFP-expressing Legionella spp. and their parental strains. This study demonstrates that the use of a GFP-expressing plasmid can serve as a viable approach for investigating Legionella non-pneumophila spp. in real time.


2016 ◽  
Vol 136 (5) ◽  
pp. S2
Author(s):  
S.J. Balin ◽  
S. Stenger ◽  
M. Pellegrni ◽  
M. Ochoa ◽  
M. Schenk ◽  
...  

2000 ◽  
Vol 11 (1) ◽  
pp. 153-160 ◽  
Author(s):  
Belinda S. Hall ◽  
Winnie Tam ◽  
Ranjan Sen ◽  
Miercio E. A. Pereira

The transcription factor nuclear factor-κB (NF-κB) is central to the innate and acquired immune response to microbial pathogens, coordinating cellular responses to the presence of infection. Here we demonstrate a direct role for NF-κB activation in controlling intracellular infection in nonimmune cells. Trypanosoma cruzi is an intracellular parasite of mammalian cells with a marked preference for infection of myocytes. The molecular basis for this tissue tropism is unknown. Trypomastigotes, the infectious stage of T. cruzi, activate nuclear translocation and DNA binding of NF-κB p65 subunit and NF-κB-dependent gene expression in epithelial cells, endothelial cells, and fibroblasts. Inactivation of epithelial cell NF-κB signaling by inducible expression of the inhibitory mutant IκBaM significantly enhances parasite invasion.T. cruzi do not activate NF-κB in cells derived from skeletal, smooth, or cardiac muscle, despite the ability of these cells to respond to tumor necrosis factor-α with NF-κB activation. The in vitro infection level in these muscle-derived cells is more than double that seen in the other cell types tested. Therefore, the ability of T. cruzi to activate NF-κB correlates inversely with susceptibility to infection, suggesting that NF-κB activation is a determinant of the intracellular survival and tissue tropism ofT. cruzi.


2001 ◽  
Vol 6 (1) ◽  
pp. 59 ◽  
Author(s):  
Peter J. Mark ◽  
Bryan K. Ward ◽  
Premlata Kumar ◽  
Hooshang Lahooti ◽  
Rodney F. Minchin ◽  
...  

2012 ◽  
Vol 205 (10) ◽  
pp. 1617-1618
Author(s):  
Sebastian Schroecksnadel ◽  
Katharina Kurz ◽  
Guenter Weiss ◽  
Dietmar Fuchs

2017 ◽  
Vol 13 (5) ◽  
pp. e1006363 ◽  
Author(s):  
Amy K. Barczak ◽  
Roi Avraham ◽  
Shantanu Singh ◽  
Samantha S. Luo ◽  
Wei Ran Zhang ◽  
...  

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