Rubicon-Dependent Lc3 Recruitment to Salmonella-Containing Phagosomes Is a Host Defense Mechanism Triggered Independently From Major Bacterial Virulence Factors

In order to cause disease on plants, gram-negative phytopathogenic bacteria introduce numerous virulence factors into the host cell in order to render host tissue more hospitable for pathogen proliferation. The mode of action of such bacterial virulence factors and their interaction with host defense pathways remain poorly understood. avrRpt2, a gene from Pseudomonas syringae pv. tomato JL1065, has been shown to promote the virulence of heterologous P. syringae strains on Arabidopsis thaliana. However, the contribution of avrRpt2 to the virulence of JL1065 has not been examined previously. We show that a mutant derivative of JL1065 that carries a disruption in avrRpt2 is impaired in its ability to cause disease on tomato (Lycopersicon esculentum), indicating that avrRpt2 also acts as a virulence gene in its native strain on a natural host. The virulence activity of avrRpt2 was detectable on tomato lines that are defective in either ethylene perception or the accumulation of salicylic acid, but could not be detected on a tomato mutant insensitive to jasmonic acid. The enhanced virulence conferred by the expression of avrRpt2 in JL1065 was not associated with the suppression of several defense-related genes induced during the infection of tomato.

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Human Serum Albumin Is an Essential Component of the Host Defense Mechanism Against Clostridium difficile Intoxication

The Journal of Infectious Diseases ◽

10.1093/infdis/jiy338 ◽

2018 ◽

Vol 218 (9) ◽

pp. 1424-1435 ◽

Cited By ~ 15

Author(s):

Alessandra di Masi ◽

Loris Leboffe ◽

Fabio Polticelli ◽

Federica Tonon ◽

Cristina Zennaro ◽

...

Keyword(s):

Clostridium Difficile ◽

Human Serum Albumin ◽

Serum Albumin ◽

Human Serum ◽

Host Defense ◽

Defense Mechanism ◽

Essential Component ◽

Host Defense Mechanism

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Fever as a Host Defense Mechanism

The Brain and Host Defense - NeuroImmune Biology ◽

10.1016/s1567-7443(10)70023-5 ◽

2010 ◽

pp. 213-235 ◽

Cited By ~ 3

Author(s):

Clark M. Blatteis

Keyword(s):

Host Defense ◽

Defense Mechanism ◽

Host Defense Mechanism

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Autophagy-activating strategies to promote innate defense against mycobacteria

Experimental & Molecular Medicine ◽

10.1038/s12276-019-0290-7 ◽

2019 ◽

Vol 51 (12) ◽

pp. 1-10 ◽

Cited By ~ 12

Author(s):

Yi Sak Kim ◽

Prashanta Silwal ◽

Soo Yeon Kim ◽

Tamotsu Yoshimori ◽

Eun-Kyeong Jo

Keyword(s):

Host Defense ◽

Defense Mechanism ◽

Multidrug Resistant ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

Innate Defense ◽

Host Defense Mechanism ◽

A Cell

AbstractMycobacterium tuberculosis (Mtb) is a major causal pathogen of human tuberculosis (TB), which is a serious health burden worldwide. The demand for the development of an innovative therapeutic strategy to treat TB is high due to drug-resistant forms of TB. Autophagy is a cell-autonomous host defense mechanism by which intracytoplasmic cargos can be delivered and then destroyed in lysosomes. Previous studies have reported that autophagy-activating agents and small molecules may be beneficial in restricting intracellular Mtb infection, even with multidrug-resistant Mtb strains. Recent studies have revealed the essential roles of host nuclear receptors (NRs) in the activation of the host defense through antibacterial autophagy against Mtb infection. In particular, we discuss the function of estrogen-related receptor (ERR) α and peroxisome proliferator-activated receptor (PPAR) α in autophagy regulation to improve host defenses against Mtb infection. Despite promising findings relating to the antitubercular effects of various agents, our understanding of the molecular mechanism by which autophagy-activating agents suppress intracellular Mtb in vitro and in vivo is lacking. An improved understanding of the antibacterial autophagic mechanisms in the innate host defense will eventually lead to the development of new therapeutic strategies for human TB.

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Pathogenesis of thrombosis

Hematology ◽

10.1182/asheducation-2009.1.255 ◽

2009 ◽

Vol 2009 (1) ◽

pp. 255-258 ◽

Cited By ~ 15

Author(s):

Bruce Furie

Keyword(s):

High Pressure ◽

Host Defense ◽

Intravital Microscopy ◽

Defense Mechanism ◽

Tissue Injury ◽

Thrombus Formation ◽

Animal Experiments ◽

Circulatory System ◽

Live Animal ◽

Host Defense Mechanism

Abstract The hemostatic process is a host defense mechanism to preserve the integrity of the closed high pressure circulatory system. This process must remain inactive but poised to minimize extravasation of blood from the vasculature following tissue injury. Given the complexity of the hemostatic mechanism, paradigms developed from biochemical and cell biological approaches have been revisited by studying thrombus formation in a live animal by intravital microscopy. Many of these paradigms have proven accurate, but others need to be reconsidered given the results of whole animal experiments.

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