scholarly journals Human Cytomegalovirus IE1 Protein Elicits a Type II Interferon-Like Host Cell Response That Depends on Activated STAT1 but Not Interferon-γ

2011 ◽  
Vol 7 (4) ◽  
pp. e1002016 ◽  
Author(s):  
Theresa Knoblach ◽  
Benedikt Grandel ◽  
Jana Seiler ◽  
Michael Nevels ◽  
Christina Paulus
Keyword(s):  
Host Cell ◽  
Human Cytomegalovirus ◽  
Cell Response ◽  
Interferon Γ ◽  
Type Ii ◽  
Host Cell Response

scholarly journals Defective Interfering RNA Viruses and the Host-Cell Response

1980 ◽  
pp. 137-192 ◽  
Author(s):  
John J. Holland ◽  
S. Ian T. Kennedy ◽  
Bert L. Semler ◽  
Charlotte L. Jones ◽  
Laurent Roux ◽  
...  
Keyword(s):  
Host Cell ◽  
Cell Response ◽  
Rna Viruses ◽  
Host Cell Response ◽  
Defective Interfering Rna ◽  
Interfering Rna

scholarly journals Pore Formation Triggered by Legionella spp. Is an Nlrc4 Inflammasome-Dependent Host Cell Response That Precedes Pyroptosis

2010 ◽  
Vol 78 (3) ◽  
pp. 1403-1413 ◽  
Author(s):  
Tatiana N. Silveira ◽  
Dario S. Zamboni
Keyword(s):  
Host Cell ◽  
Legionella Pneumophila ◽  
Cell Response ◽  
Pore Formation ◽  
De Novo ◽  
Membrane Damage ◽  
Secretion System ◽  
Cell Permeabilization ◽  
Host Cell Response ◽  
Caspase 1

ABSTRACT Legionella pneumophila, the etiological agent of Legionnaires disease, is known to trigger pore formation in bone marrow-derived macrophages (BMMs) by mechanisms dependent on the type IVB secretion system known as Dot/Icm. Here, we used several mutants of L. pneumophila in combination with knockout mice to assess the host and bacterial factors involved in pore formation in BMMs. We found that regardless of Dot/Icm activity, pore formation does not occur in BMMs deficient in caspase-1 and Nlrc4/Ipaf. Pore formation was temporally associated with interleukin-1β secretion and preceded host cell lysis and pyroptosis. Pore-forming ability was dependent on bacterial Dot/Icm but independent of several effector proteins, multiplication, and de novo protein synthesis. Flagellin, which is known to trigger the Nlrc4 inflammasome, was required for pore formation as flaA mutant bacteria failed to induce cell permeabilization. Accordingly, transfection of purified flagellin was sufficient to trigger pore formation independent of infection. By using 11 different Legionella species, we found robust pore formation in response to L. micdadei, L. bozemanii, L. gratiana, L. jordanis, and L. rubrilucens, and this trait correlated with flagellin expression by these species. Together, the results suggest that pore formation is neither L. pneumophila specific nor the result of membrane damage induced by Dot/Icm activity; instead, it is a highly coordinated host cell response dependent on host Nlrc4 and caspase-1 and on bacterial flagellin and type IV secretion system.

scholarly journals Trypanosoma cruzi Infection Induces a Global Host Cell Response in Cardiomyocytes

2011 ◽  
Vol 79 (8) ◽  
pp. 3471-3471 ◽  
Author(s):  
Patricio A. Manque ◽  
Christian M. Probst ◽  
Mirian C. S. Pereira ◽  
Rita C. P. Rampazzo ◽  
Luiz Shozo Ozaki ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Host Cell ◽  
Cell Response ◽  
Host Cell Response ◽  
Cruzi Infection

Real-time impedance analysis of host cell response to meningococcal infection

2011 ◽  
Vol 84 (1) ◽  
pp. 101-108 ◽  
Author(s):  
H. Slanina ◽  
A. König ◽  
H. Claus ◽  
M. Frosch ◽  
A. Schubert-Unkmeir
Keyword(s):  
Host Cell ◽  
Real Time ◽  
Cell Response ◽  
Impedance Analysis ◽  
Meningococcal Infection ◽  
Host Cell Response

scholarly journals Motor properties of PilT-independent type 4 pilus retraction in gonococci

2018 ◽  
Author(s):  
Robert Zöllner ◽  
Tom Cronenberg ◽  
Berenike Maier
Keyword(s):  
Host Cell ◽  
Cell Response ◽  
Molecular Machines ◽  
Proton Motive Force ◽  
Motive Force ◽  
Maximum Force ◽  
Twitching Motility ◽  
Host Cell Response ◽  
Bacterial Type

Bacterial type 4 pili (T4P) belong to the strongest molecular machines. The gonococcal T4P retraction ATPase PilT supports forces exceeding 100 pN during T4P retraction. Here, we address the question whether gonococcal T4P retract in the absence of PilT. We show that pilT deletion strains indeed retract their T4P but the maximum force is reduced to 5 pN. Similarly, the speed of T4P retraction is lower by orders of magnitude compared to T4P retraction driven by PilT. Deleting the pilT paralogues pilU and pilT2 in the DpilT background did not inhibit T4P retraction, indicating that the PilT-like proteins do not compensate for PilT. Furthermore, we show that depletion of proton motive force did not inhibit pilT-independent T4P retraction. We conclude that the retraction ATPase is not essential for gonococcal T4P retraction. However, the force generated in the absence of PilT is too low to support important functions of T4P including twitching motility, fluidization of colonies, or induction of host cell response.

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