scholarly journals Persistent production of interferon-gamma (IFN-γ) and IL-12 is essential for the generation of protective immunity against Listeria monocytogenes

1997 ◽  
Vol 108 (3) ◽  
pp. 456-462 ◽  
Author(s):  
H. XIONG ◽  
S. OHYA ◽  
Y. TANABE ◽  
M. MITSUYAMA
Keyword(s):  
Listeria Monocytogenes ◽  
Interferon Gamma ◽  
Protective Immunity ◽  
Ifn Γ

scholarly journals Macrophage Depletion Prior to Neospora caninum Infection Results in Severe Neosporosis in Mice

2014 ◽  
Vol 21 (8) ◽  
pp. 1185-1188 ◽  
Author(s):  
Chisa Abe ◽  
Sachi Tanaka ◽  
Fumiaki Ihara ◽  
Yoshifumi Nishikawa
Keyword(s):  
Interferon Gamma ◽  
Interleukin 6 ◽  
Protective Immunity ◽  
Neospora Caninum ◽  
Caninum Infection ◽  
Content Type ◽  
Murine Macrophages ◽  
Macrophage Depletion ◽  
Increased Sensitivity ◽  
Ifn Γ

ABSTRACTWe observed that murine macrophages showed greater activation and increased interleukin 6 (IL-6), IL-12p40, and interferon gamma (IFN-γ) production duringNeospora caninuminfection. Many macrophages migrated to the site of infection. Furthermore, macrophage-depleted mice exhibited increased sensitivity toN. caninuminfection. This study indicates that macrophages are required for achieving protective immunity againstN. caninum.

scholarly journals A Role for IFN-γ from Antigen-Specific CD8+ T Cells in Protective Immunity to Listeria monocytogenes

2007 ◽  
Vol 179 (4) ◽  
pp. 2457-2466 ◽  
Author(s):  
Kelly A. N. Messingham ◽  
Vladimir P. Badovinac ◽  
Ali Jabbari ◽  
John T. Harty
Keyword(s):  
T Cells ◽  
Listeria Monocytogenes ◽  
Cd8 T Cells ◽  
Protective Immunity ◽  
Ifn Γ

scholarly journals Cytolysin-Dependent Escape of the Bacterium from the Phagosome Is Required but Not Sufficient for Induction of the Th1 Immune Response against Listeria monocytogenes Infection: Distinct Role of Listeriolysin O Determined by Cytolysin Gene Replacement

2007 ◽  
Vol 75 (8) ◽  
pp. 3791-3801 ◽  
Author(s):  
Hideki Hara ◽  
Ikuo Kawamura ◽  
Takamasa Nomura ◽  
Takanari Tominaga ◽  
Kohsuke Tsuchiya ◽  
...  
Keyword(s):  
Immune Response ◽  
Listeria Monocytogenes ◽  
Virulence Factor ◽  
Protective Immunity ◽  
Gene Replacement ◽  
Listeriolysin O ◽  
Listeria Ivanovii ◽  
Ifn Γ

ABSTRACT Listeria monocytogenes evades the antimicrobial mechanisms of macrophages by escaping from the phagosome into the cytosolic space via a unique cytolysin that targets the phagosomal membrane, listeriolysin O (LLO), encoded by hly. Gamma interferon (IFN-γ), which is known to play a pivotal role in the induction of Th1-dependent protective immunity in mice, appears to be produced, depending on the bacterial virulence factor. To determine whether the LLO molecule (the major virulence factor of L. monocytogenes) is indispensable or the escape of bacteria from the phagosome is sufficient to induce IFN-γ production, we first constructed an hly-deleted mutant of L. monocytogenes and then established isogenic L. monocytogenes mutants expressing LLO or ivanolysin O (ILO), encoded by ilo from Listeria ivanovii. LLO-expressing L. monocytogenes was highly capable of inducing IFN-γ production and Listeria-specific protective immunity, while the hly-deleted mutant was not. In contrast, the level of IFN-γ induced by ILO-expressing L. monocytogenes was significantly lower both in vitro and in vivo, despite the ability of this strain to escape the phagosome and the intracellular multiplication at a level equivalent to that of LLO-expressing L. monocytogenes. Only a negligible level of protective immunity was induced in mice against challenge with LLO- and ILO-expressing L. monocytogenes. These results clearly show that escape of the bacterium from the phagosome is a prerequisite but is not sufficient for the IFN-γ-dependent Th1 response against L. monocytogenes, and some distinct molecular nature of LLO is indispensable for the final induction of IFN-γ that is essentially required to generate a Th1-dependent immune response.

scholarly journals Differences in Gamma Interferon Production Induced by Listeriolysin O and Ivanolysin O Result in Different Levels of Protective Immunity in Mice Infected with Listeria monocytogenes and Listeria ivanovii

2003 ◽  
Vol 71 (5) ◽  
pp. 2447-2454 ◽  
Author(s):  
Terumi Kimoto ◽  
Ikuo Kawamura ◽  
Chikara Kohda ◽  
Takamasa Nomura ◽  
Kohsuke Tsuchiya ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Protective Immunity ◽  
Lethal Dose ◽  
Gamma Interferon ◽  
Listeriolysin O ◽  
Serum Samples ◽  
Listeria Ivanovii ◽  
Ifn Γ ◽  
Different Levels

ABSTRACT Two pathogenic species in the genus Listeria, Listeria monocytogenes and Listeria ivanovii, are characterized by the production of hemolysins belonging to cholesterol-dependent cytolysins, listeriolysin O (LLO) and ivanolysin O (ILO), respectively. LLO, produced by L. monocytogenes, is able to induce gamma interferon (IFN-γ) production and contributes to the generation of Th1-dependent protective immunity. On the other hand, nothing is known about the role of ILO, produced by L. ivanovii, in this regard. In this study, we immunized mice with 0.1 50% lethal dose (LD50) of L. monocytogenes and L. ivanovii. Protective immunity against a challenge with 10 LD50 was generated in mice infected with L. monocytogenes, whereas L. ivanovii infection did not induce protection. After immunization, the level of IFN-γ in serum samples was increased in mice given L. monocytogenes but not in those given L. ivanovii. To determine the IFN-γ-inducing activity of cytolysins, recombinant protein was constructed. Recombinant ILO exhibited significantly lower IFN-γ-inducing activity than LLO. By comparing the IFN-γ-inducing activity of a chimera incorporating LLO and ILO, it was found that domains 1 to 3 of LLO were critical for IFN-γ-inducing activity while the counterpart in ILO was unable to induce cytokine production. These results suggested that the weak ability of ILO to induce IFN-γ production is responsible for the failure of L. ivanovii to generate effective protective immunity.

scholarly journals Interferon-gamma promotes iron export in human macrophages to limit intracellular bacterial replication

2020 ◽  
Author(s):  
Rodrigo Abreu ◽  
Lauren Essler ◽  
Pramod Giri ◽  
Fred Quinn
Keyword(s):  
Listeria Monocytogenes ◽  
Interferon Gamma ◽  
The United States ◽  
Intracellular Pathogens ◽  
Iron Availability ◽  
Intracellular Iron ◽  
Human Macrophages ◽  
Iron Sequestration ◽  
Ifn Γ ◽  
Iron Export

AbstractSalmonellosis and listeriosis together accounted for more than one third of foodborne illnesses in the United States and almost half the hospitalizations for gastrointestinal diseases in 2018 while tuberculosis afflicted over 10 million people worldwide causing almost 2 million deaths. Regardless of the intrinsic virulence differences among Listeria monocytogenes, Salmonella enterica and Mycobacterium tuberculosis, these intracellular pathogens share the ability to survive and persist inside the macrophage and other cells and thrive in iron rich environments. Interferon-gamma (IFN-γ) is a central cytokine in host defense against intracellular pathogens and has been shown to promote iron export in macrophages. We hypothesize that IFN-γ decreases iron availability to intracellular pathogens consequently limiting replication in these cells. In this study, we show that IFN-γ regulates the expression of iron-related proteins hepcidin, ferroportin, and ferritin to induce iron export from macrophages. Listeria monocytogenes, S. enterica, and M. tuberculosis infections significantly induce iron sequestration in human macrophages. In contrast, IFN-γ significantly reduces hepcidin secretion in S. enterica and M. tuberculosis infected macrophages. Similarly, IFN-γ-activated macrophages express higher ferroportin levels than untreated controls even after infection with L. monocytogenes bacilli; bacterial infection greatly down-regulates ferroportin expression. Collectively, IFN-γ significantly inhibits pathogen-associated intracellular iron sequestration in macrophages and consequently retards the growth of intracellular bacterial pathogens by decreasing iron availability.

scholarly journals Interferon-gamma promotes iron export in human macrophages to limit intracellular bacterial replication

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0240949
Author(s):  
Rodrigo Abreu ◽  
Lauren Essler ◽  
Pramod Giri ◽  
Frederick Quinn
Keyword(s):  
Listeria Monocytogenes ◽  
Interferon Gamma ◽  
The United States ◽  
Intracellular Pathogens ◽  
Iron Availability ◽  
Intracellular Iron ◽  
Human Macrophages ◽  
Iron Sequestration ◽  
Ifn Γ ◽  
Iron Export

Salmonellosis and listeriosis together accounted for more than one third of foodborne illnesses in the United States and almost half the hospitalizations for gastrointestinal diseases in 2018 while tuberculosis afflicted over 10 million people worldwide causing almost 2 million deaths. Regardless of the intrinsic virulence differences among Listeria monocytogenes, Salmonella enterica and Mycobacterium tuberculosis, these intracellular pathogens share the ability to survive and persist inside the macrophage and other cells and thrive in iron rich environments. Interferon-gamma (IFN-γ) is a central cytokine in host defense against intracellular pathogens and has been shown to promote iron export in macrophages. We hypothesize that IFN-γ decreases iron availability to intracellular pathogens consequently limiting replication in these cells. In this study, we show that IFN-γ regulates the expression of iron-related proteins hepcidin, ferroportin, and ferritin to induce iron export from macrophages. Listeria monocytogenes, S. enterica, and M. tuberculosis infections significantly induce iron sequestration in human macrophages. In contrast, IFN-γ significantly reduces hepcidin secretion in S. enterica and M. tuberculosis infected macrophages. Similarly, IFN-γ-activated macrophages express higher ferroportin levels than untreated controls even after infection with L. monocytogenes bacilli; bacterial infection greatly down-regulates ferroportin expression. Collectively, IFN-γ significantly inhibits pathogen-associated intracellular iron sequestration in macrophages and consequently retards the growth of intracellular bacterial pathogens by decreasing iron availability.

scholarly journals Desarrollo de la técnica de interferón gamma (IFN-γ) para la detección de bovinos infectados con Listeria monocytogenes

2015 ◽  
Vol 18 (1) ◽  
Author(s):  
Carolina Carolina Gallego ◽  
◽  
Manuel I. Gallego ◽  
José L. Azumendi ◽  
Jeimara Paipa ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Interferon Gamma ◽  
Ifn Γ

scholarly journals Circulating CD4 T cells elicited by endemic coronaviruses display vast disparities in abundance and functional potential linked to both antigen specificity and age

2021 ◽  
Author(s):  
Katherine A Richards ◽  
Maryah Glover ◽  
Jeremy C Crawford ◽  
Paul Thomas ◽  
Chantelle White ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Protective Immunity ◽  
Granzyme B ◽  
Antigen Specificity ◽  
Functional Potential ◽  
Membrane Envelope ◽  
Ifn Γ ◽  
Human Coronaviruses ◽  
Repeated Infections

Abstract Repeated infections with endemic human coronaviruses are thought to reflect lack of long-lasting protective immunity. Here, we evaluate circulating human CD4 T cells collected prior to 2020 for reactivity towards hCoV spike proteins, probing for the ability to produce IFN-γ, IL-2 or granzyme B. We find robust reactivity to spike-derived epitopes, comparable to influenza, but highly variable abundance and functional potential across subjects, depending on age and viral antigen specificity. To explore the potential of these memory cells to be recruited in SARS-CoV-2 infection, we examined the same subjects for cross-reactive recognition of epitopes from SARS-CoV-2 nucleocapsid, membrane/envelope, and spike. The functional potential of these cross-reactive CD4 T cells was highly variable, with nucleocapsid-specific CD4 T cells, but not spike-reactive cells showing exceptionally high levels of granzyme production upon stimulation. These results are considered in light of recruitment of hCoV-reactive cells into responses of humans to SARS-CoV infections or vaccinations.

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