scholarly journals The root endophytic fungus Piriformospora indica requires host cell death for proliferation during mutualistic symbiosis with barley

2006 ◽  
Vol 103 (49) ◽  
pp. 18450-18457 ◽  
Author(s):  
S. Deshmukh ◽  
R. Huckelhoven ◽  
P. Schafer ◽  
J. Imani ◽  
M. Sharma ◽  
...  
Keyword(s):  
Cell Death ◽  
Host Cell ◽  
Endophytic Fungus ◽  
Piriformospora Indica ◽  
Mutualistic Symbiosis ◽  
Host Cell Death

scholarly journals Pathogen induced subversion of NAD+ metabolism mediating host cell death: a target for development of chemotherapeutics

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ayushi Chaurasiya ◽  
Swati Garg ◽  
Ashish Khanna ◽  
Chintam Narayana ◽  
Ved Prakash Dwivedi ◽  
...  
Keyword(s):  
Cell Death ◽  
Host Cell ◽  
Nicotinamide Adenine Dinucleotide ◽  
Malaria Parasite ◽  
Host Cells ◽  
Nicotinamide Adenine ◽  
Targeted Therapeutics ◽  
Nad Metabolism ◽  
Host Cell Death ◽  
Nanomolar Range

AbstractHijacking of host metabolic status by a pathogen for its regulated dissemination from the host is prerequisite for the propagation of infection. M. tuberculosis secretes an NAD+-glycohydrolase, TNT, to induce host necroptosis by hydrolyzing Nicotinamide adenine dinucleotide (NAD+). Herein, we expressed TNT in macrophages and erythrocytes; the host cells for M. tuberculosis and the malaria parasite respectively, and found that it reduced the NAD+ levels and thereby induced necroptosis and eryptosis resulting in premature dissemination of pathogen. Targeting TNT in M. tuberculosis or induced eryptosis in malaria parasite interferes with pathogen dissemination and reduction in the propagation of infection. Building upon our discovery that inhibition of pathogen-mediated host NAD+ modulation is a way forward for regulation of infection, we synthesized and screened some novel compounds that showed inhibition of NAD+-glycohydrolase activity and pathogen infection in the nanomolar range. Overall this study highlights the fundamental importance of pathogen-mediated modulation of host NAD+ homeostasis for its infection propagation and novel inhibitors as leads for host-targeted therapeutics.

scholarly journals TolC-Dependent Modulation of Host Cell Death by the Francisella tularensis Live Vaccine Strain

2014 ◽  
Vol 82 (5) ◽  
pp. 2068-2078 ◽  
Author(s):  
Christopher R. Doyle ◽  
Ji-An Pan ◽  
Patricio Mena ◽  
Wei-Xing Zong ◽  
David G. Thanassi
Keyword(s):  
Cell Death ◽  
Immune Responses ◽  
Host Cell ◽  
Francisella Tularensis ◽  
Vaccine Strain ◽  
Live Vaccine ◽  
Live Vaccine Strain ◽  
Type I ◽  
Content Type ◽  
Host Cell Death

ABSTRACTFrancisella tularensisis a facultative intracellular, Gram-negative pathogen and the causative agent of tularemia. We previously identified TolC as a virulence factor of theF. tularensislive vaccine strain (LVS) and demonstrated that a ΔtolCmutant exhibits increased cytotoxicity toward host cells and elicits increased proinflammatory responses compared to those of the wild-type (WT) strain. TolC is the outer membrane channel component used by the type I secretion pathway to export toxins and other bacterial virulence factors. Here, we show that the LVS delays activation of the intrinsic apoptotic pathway in a TolC-dependent manner, both during infection of primary macrophages and during organ colonization in mice. The TolC-dependent delay in host cell death is required forF. tularensisto preserve its intracellular replicative niche. We demonstrate that TolC-mediated inhibition of apoptosis is an active process and not due to defects in the structural integrity of the ΔtolCmutant. These findings support a model wherein the immunomodulatory capacity ofF. tularensisrelies, at least in part, on TolC-secreted effectors. Finally, mice vaccinated with the ΔtolCLVS are protected from lethal challenge and clear challenge doses faster than WT-vaccinated mice, demonstrating that the altered host responses to primary infection with the ΔtolCmutant led to altered adaptive immune responses. Taken together, our data demonstrate that TolC is required for temporal modulation of host cell death during infection byF. tularensisand highlight how shifts in the magnitude and timing of host innate immune responses may lead to dramatic changes in the outcome of infection.

Fusarium graminearum produces different xylanases causing host cell death that is prevented by the xylanase inhibitors XIP-I and TAXI-III in wheat

Plant Science ◽  
2015 ◽  
Vol 240 ◽  
pp. 161-169 ◽  
Author(s):  
Silvio Tundo ◽  
Ilaria Moscetti ◽  
Franco Faoro ◽  
Mickaël Lafond ◽  
Thierry Giardina ◽  
...  
Keyword(s):  
Cell Death ◽  
Host Cell ◽  
Fusarium Graminearum ◽  
Host Cell Death

scholarly journals Pattern Recognition Receptors and the Host Cell Death Molecular Machinery

2018 ◽  
Vol 9 ◽  
Author(s):  
Gustavo P. Amarante-Mendes ◽  
Sandy Adjemian ◽  
Laura Migliari Branco ◽  
Larissa C. Zanetti ◽  
Ricardo Weinlich ◽  
...  
Keyword(s):  
Pattern Recognition ◽  
Cell Death ◽  
Host Cell ◽  
Pattern Recognition Receptors ◽  
Host Cell Death ◽  
Molecular Machinery

scholarly journals Modulation of Host Cell Death by SARS Coronavirus Proteins

2009 ◽  
pp. 231-245 ◽  
Author(s):  
Claudia Diemer ◽  
Martha Schneider ◽  
Hermann M. Schätzl ◽  
Sabine Gilch
Keyword(s):  
Cell Death ◽  
Host Cell ◽  
Sars Coronavirus ◽  
Host Cell Death
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