Reduced in vivo Nonspecific Resistance to Listeria monocytogenes Infection during Avian Retrovirus-Induced Immunosuppression

1988 ◽  
Vol 32 (4) ◽  
pp. 663 ◽  
Author(s):  
T. J. Cummins ◽  
I. M. Orme ◽  
R. E. Smith
Keyword(s):  
Listeria Monocytogenes ◽  
Nonspecific Resistance ◽  
Listeria Monocytogenes Infection

scholarly journals The in vivo ISGylome links ISG15 to metabolic pathways and autophagy upon Listeria monocytogenes infection

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Yifeng Zhang ◽  
Fabien Thery ◽  
Nicholas C. Wu ◽  
Emma K. Luhmann ◽  
Olivier Dussurget ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Metabolic Pathways ◽  
Quantitative Proteomics ◽  
Computational Analysis ◽  
Murine Models ◽  
Direct Modification ◽  
Catalytic Sites ◽  
Listeria Monocytogenes Infection

AbstractISG15 is an interferon-stimulated, ubiquitin-like protein, with anti-viral and anti-bacterial activity. Here, we map the endogenous in vivo ISGylome in the liver following Listeria monocytogenes infection by combining murine models of reduced or enhanced ISGylation with quantitative proteomics. Our method identifies 930 ISG15 sites in 434 proteins and also detects changes in the host ubiquitylome. The ISGylated targets are enriched in proteins which alter cellular metabolic processes, including upstream modulators of the catabolic and antibacterial pathway of autophagy. Computational analysis of substrate structures reveals that a number of ISG15 modifications occur at catalytic sites or dimerization interfaces of enzymes. Finally, we demonstrate that animals and cells with enhanced ISGylation have increased basal and infection-induced autophagy through the modification of mTOR, WIPI2, AMBRA1, and RAB7. Taken together, these findings ascribe a role of ISGylation to temporally reprogram organismal metabolism following infection through direct modification of a subset of enzymes in the liver.

scholarly journals Commensal microbes provide first line defense against Listeria monocytogenes infection

2017 ◽  
Vol 214 (7) ◽  
pp. 1973-1989 ◽  
Author(s):  
Simone Becattini ◽  
Eric R. Littmann ◽  
Rebecca A. Carter ◽  
Sohn G. Kim ◽  
Sejal M. Morjaria ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Intestinal Microbiota ◽  
Systemic Disease ◽  
Foodborne Pathogen ◽  
Antibiotic Administration ◽  
Defensive Role ◽  
Listeria Monocytogenes Infection ◽  
Dose Oral

Listeria monocytogenes is a foodborne pathogen that causes septicemia, meningitis and chorioamnionitis and is associated with high mortality. Immunocompetent humans and animals, however, can tolerate high doses of L. monocytogenes without developing systemic disease. The intestinal microbiota provides colonization resistance against many orally acquired pathogens, and antibiotic-mediated depletion of the microbiota reduces host resistance to infection. Here we show that a diverse microbiota markedly reduces Listeria monocytogenes colonization of the gut lumen and prevents systemic dissemination. Antibiotic administration to mice before low dose oral inoculation increases L. monocytogenes growth in the intestine. In immunodeficient or chemotherapy-treated mice, the intestinal microbiota provides nonredundant defense against lethal, disseminated infection. We have assembled a consortium of commensal bacteria belonging to the Clostridiales order, which exerts in vitro antilisterial activity and confers in vivo resistance upon transfer into germ free mice. Thus, we demonstrate a defensive role of the gut microbiota against Listeria monocytogenes infection and identify intestinal commensal species that, by enhancing resistance against this pathogen, represent potential probiotics.

Prevention of the enhancing effect of mucin and iron in mouse meningococcal infection

1983 ◽  
Vol 29 (12) ◽  
pp. 1671-1674 ◽  
Author(s):  
J. M. Dupuy ◽  
B. G. Sparkes ◽  
M. Desrosiers ◽  
E. Skamene ◽  
V. V. Micusan
Keyword(s):  
Listeria Monocytogenes ◽  
Neisseria Meningitidis ◽  
Crude Extract ◽  
Concomitant Administration ◽  
Reticuloendothelial System ◽  
Meningococcal Infection ◽  
Nonspecific Resistance ◽  
Enhancing Effect ◽  
Proteose Peptone

In vivo resistance of mice to Neisseria meningitidis was entirely abrogated by a concomitant administration of mucin and iron with N. meningitidis organisms. Resistance, however, was restored when the latter challenge was given to animals which had been immunized 7 days previously with a crude extract of meningococcal antigens (MA), BCG, or proteose peptone. These results suggest that depression or activation of the reticuloendothelial system (RES) may be important in resistant of mice to meningococcal infection. Also, like BCG, MA inoculation was able to prevent infection by Listeria monocytogenes indicating its marked ability to activate the RES. The data show that immunization can induce nonspecific RES stimulation and that the nonspecific resistance persists for at least 7 days.

scholarly journals ADAP Promotes Degranulation and Migration of NK Cells Primed During in vivo Listeria monocytogenes Infection in Mice

2020 ◽  
Vol 10 ◽  
Author(s):  
Martha A. L. Böning ◽  
Stephanie Trittel ◽  
Peggy Riese ◽  
Marco van Ham ◽  
Maxi Heyner ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Nk Cells ◽  
Listeria Monocytogenes Infection ◽  
And Migration

scholarly journals The cell biology of Listeria monocytogenes infection

2002 ◽  
Vol 158 (3) ◽  
pp. 409-414 ◽  
Author(s):  
Daniel A. Portnoy ◽  
Victoria Auerbuch ◽  
Ian J. Glomski
Keyword(s):  
Listeria Monocytogenes ◽  
Host Cell ◽  
Cell Biology ◽  
Productive Infection ◽  
Acquired Immunity ◽  
Listeriolysin O ◽  
Listeria Monocytogenes Infection ◽  
Infected Cells ◽  
Fail Safe

Listeria monocytogenes has emerged as a remarkably tractable pathogen to dissect basic aspects of cell biology, intracellular pathogenesis, and innate and acquired immunity. In order to maintain its intracellular lifestyle, L. monocytogenes has evolved a number of mechanisms to exploit host processes to grow and spread cell to cell without damaging the host cell. The pore-forming protein listeriolysin O mediates escape from host vacuoles and utilizes multiple fail-safe mechanisms to avoid causing toxicity to infected cells. Once in the cytosol, the L. monocytogenes ActA protein recruits host cell Arp2/3 complexes and enabled/vasodilator-stimulated phosphoprotein family members to mediate efficient actin-based motility, thereby propelling the bacteria into neighboring cells. Alteration in any of these processes dramatically reduces the ability of the bacteria to establish a productive infection in vivo.

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