Faculty Opinions recommendation of IFN-γ production by CD27⁺ NK cells exacerbates Listeria monocytogenes infection in mice by inhibiting granulocyte mobilization.

Bovine lactoferrin (BLf) and its derivative peptide lactoferricin B (LfcinB) are known for their antimicrobial activity towards several pathogens, including Listeria monocytogenes, a food-borne Gram-positive invasive bacterium that infects a wide variety of host cells, including professional phagocytes. To add further information on the antibacterial effects of these compounds, the influence of BLf, LfcinB and the antimicrobial centre of LfcinB, the hexapeptide LfcinB4–9, on the invasive behaviour of L. monocytogenes was analysed in IFN-γ-activated human macrophagic cells (THP-1). Significant inhibition of bacterial entry in THP-1 cells was observed at LfcinB concentrations that were unable to produce any bacteriostatic or bactericidal effect, compared with BLf and LfcinB4–9 peptide. This inhibition occurred when LfcinB was incubated during the bacterial infection step and was not due only to competition for common glycosaminoglycan receptors. Assays performed through a temperature shift from 4 to 37 °C showed that inhibition of invasion took place at an early post-adsorption step, although an effect on a different step of intracellular infection could not be ruled out.

Download Full-text

IL-12 and Type-I IFN Synergize for IFN-γ Production by CD4 T Cells, Whereas Neither Are Required for IFN-γ Production by CD8 T Cells after Listeria monocytogenes Infection

The Journal of Immunology ◽

10.4049/jimmunol.178.7.4498 ◽

2007 ◽

Vol 178 (7) ◽

pp. 4498-4505 ◽

Cited By ~ 59

Author(s):

Sing Sing Way ◽

Colin Havenar-Daughton ◽

Ganesh A. Kolumam ◽

Nural N. Orgun ◽

Kaja Murali-Krishna

Keyword(s):

T Cells ◽

Listeria Monocytogenes ◽

Cd8 T Cells ◽

Cd4 T Cells ◽

Type I ◽

Type I Ifn ◽

Listeria Monocytogenes Infection ◽

Ifn Γ

Download Full-text

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

Frontiers in Immunology ◽

10.3389/fimmu.2019.03144 ◽

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

Download Full-text

Valproic acid inhibits interferon-γ production by NK cells and increases susceptibility to Listeria monocytogenes infection

Scientific Reports ◽

10.1038/s41598-020-74836-w ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Rodolfo Soria-Castro ◽

Alma D. Chávez-Blanco ◽

Blanca Estela García-Pérez ◽

Isabel Wong-Baeza ◽

Raúl Flores-Mejía ◽

...

Keyword(s):

Valproic Acid ◽

Listeria Monocytogenes ◽

Nk Cells ◽

Cell Activation ◽

Nk Cell ◽

Bacterial Load ◽

Interferon Γ ◽

Ifn Γ ◽

Vitro Analysis

Abstract Valproic acid (VPA) is a drug commonly used for epileptic seizure control. Recently, it has been shown that VPA alters the activation of several immune cells, including Natural Killer (NK) cells, which play an important role in the containment of viruses and intracellular bacteria. Although VPA can increase susceptibility to extracellular pathogens, it is unknown whether the suppressor effect of VPA could affect the course of intracellular bacterial infection. This study aimed to evaluate the role of VPA during Listeria monocytogenes (L.m) infection, and whether NK cell activation was affected. We found that VPA significantly augmented mortality in L.m infected mice. This effect was associated with increased bacterial load in the spleen, liver, and blood. Concurrently, decreased levels of IFN-γ in serum and lower splenic indexes were observed. Moreover, in vitro analysis showed that VPA treatment decreased the frequency of IFN-γ-producing NK cells within L.m infected splenocytes. Similarly, VPA inhibited the production of IFN-γ by NK cells stimulated with IL-12 and IL-18, which is a crucial system for early IFN-γ production in listeriosis. Finally, VPA decreased the phosphorylation of STAT4, p65, and p38, without affecting the expression of IL-12 and IL-18 receptors. Altogether, our results indicate that VPA increases the susceptibility to Listeria monocytogenes infection and suggest that NK cell is one of the main targets of VPA, but further work is needed to ascertain this effect.

Download Full-text

Listeria monocytogenes infection enhances the interaction between rat non-classical MHC-Ib molecule and Ly49 receptors

Innate Immunity ◽

10.1177/1753425918759589 ◽

2018 ◽

Vol 24 (4) ◽

pp. 252-261 ◽

Cited By ~ 1

Author(s):

Hamid Shegarfi ◽

Kevin P Kane ◽

Janne Nestvold

Keyword(s):

Listeria Monocytogenes ◽

In Vitro Model ◽

Cell Function ◽

Nk Cell ◽

Mhc I ◽

Listeria Monocytogenes Infection ◽

Infected Cells ◽

Ifn Γ ◽

Vitro Model

Murine NK cell Ly49 receptors, functionally analogous to KIRs in humans recognize MHC class I molecules and play a key role in controlling NK cell function. We have previously shown that the paired activating Ly49s4 and inhibitory Ly49i4 receptors recognize undefined non-classical MHC-Ib ligands from the RT1-CE region in rats. Here, the RT1-CE16 gene of the RT1d haplotype was stably transfected into the mouse RAW macrophage cell line, termed RAW-CE16d cells. Combining RAW-CE16d cells with Ly49 expressing reporter cells demonstrated Ly49i4 and Ly49s4 specificity for CE16d. The Ly49s4/i4:CE16d interaction was confirmed by specific MHC-I blocking monoclonal Abs. Further, we used our in vitro model to study the effect of Listeria monocytogenes (LM) on CE16d after infection. LM infection and IFN-γ stimulation both led to enhanced CE16d expression on the surface of transfected RAW-CE16d cells. Interestingly, the reporter cells displayed increased response to LM-infected RAW-CE16d cells compared with IFN-γ-treated RAW-CE16d cells, suggesting a fundamental difference between these stimuli in supporting enhanced Ly49 recognition of CE16d. Collectively, our data show that Ly49s4 and Ly49i4 recognize the non-classical RT1-CE16d molecule, which in turn is up-regulated during LM infection and thereby may contribute to NK-mediated responses against infected cells.

Download Full-text

Neural Route of Cerebral Listeria monocytogenes Murine Infection: Role of Immune Response Mechanisms in Controling Bacterial Neuroinvasion

Infection and Immunity ◽

10.1128/iai.69.2.1093-1100.2001 ◽

2001 ◽

Vol 69 (2) ◽

pp. 1093-1100 ◽

Cited By ~ 41

Author(s):

Yuxuan Jin ◽

Lone Dons ◽

Krister Kristensson ◽

Martı́n E. Rottenberg

Keyword(s):

Listeria Monocytogenes ◽

Nk Cells ◽

Receptor Gene ◽

Protective Role ◽

Pathologic Features ◽

Ifn Γ ◽

Rag 1 ◽

The Brain ◽

Deficient Mice

ABSTRACT The pathologic features of cerebral Listeria monocytogenes infection strongly suggest that besides hematogenous spread, bacteria might also spread via a neural route. We propose that after snout infection of recombination activating gene 1 (RAG-1)-deficient mice, L. monocytogenesspreads to the brain via a neural route. The neural route of invasion is suggested by (i) the immunostaining of L. monocytogenesin the trigeminal ganglia (TG) and brain stem but not in other areas of the brain; (ii) the kinetics of bacterial loads in snout, TG, and brain; and (iii) the increased resistance of mice infected with aplcB bacterial mutant (unable to spread from cell to cell). Gamma interferon (IFN-γ) plays a protective role in neuroinvasion; inducible nitric oxide synthase (iNOS) accounts only partially for the protection, as shown by a comparison of the susceptibilities of IFN-γ receptor (IFN-γR)-deficient, iNOS-deficient, and wild-type mice to snout infection with L. monocytogenes. The dramatically enhanced susceptibility of RAG-1-deficient, IFN-γR gene-deficient mice indicated the overall importance of innate immune cells in the release of protective levels of IFN-γ. The source of IFN-γ appeared to be NK cells, as shown by use ofRAG-1-deficient, γ-chain receptor gene-deficient mice; NK cells played a relevant protective role in neuroinvasion through a perforin-independent mechanism. In vitro evidence indicated that IFN-γ can directly induce bacteriostatic mechanisms in neural tissue.

Download Full-text