Lactoferricin influences early events of Listeria monocytogenes infection in THP-1 human macrophages

2004 ◽  
Vol 53 (2) ◽  
pp. 87-91 ◽  
Author(s):  
Catia Longhi ◽  
Maria P. Conte ◽  
Michela Penta ◽  
Alessia Cossu ◽  
Giovanni Antonini ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Temperature Shift ◽  
Bactericidal Effect ◽  
Significant Inhibition ◽  
Host Cells ◽  
Bovine Lactoferrin ◽  
Antibacterial Effects ◽  
Food Borne ◽  
Listeria Monocytogenes Infection ◽  
Ifn Γ

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.

Apoptotic Death of Listeria Monocytogenes-Infected Human Macrophages Induced by Lactoferricin B, A Bovine Lactoferrin-Derived Peptide

2005 ◽  
Vol 18 (2) ◽  
pp. 317-325 ◽  
Author(s):  
C. Longhi ◽  
M. P. Conte ◽  
S. Ranaldi ◽  
M. Penta ◽  
P. Valenti ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Bovine Milk ◽  
Cell Types ◽  
Bovine Lactoferrin ◽  
Human Macrophages ◽  
Apoptotic Death ◽  
Food Borne ◽  
Ifn Γ

Listeria monocytogenes, an intracellular facultative food-borne pathogen, was reported to induce apoptosis in vitro and in vivo in a variety of cell types with the exception of murine macrophages. These cells represent the predominant compartment of bacterial multiplication and die as a result of necrosis. In this study we showed that human non-activated and IFN-γ-activated macrophagic-like (THP-1) cells infected with L. monocytogenes, mainly die by necrosis rather than by an apoptotic process. Two natural products derived from bovine milk, lactoferrin and its derivative peptide lactoferricin B, are capable of regulating the fate of infected human macrophages. Bovine lactoferrin treatment of macrophages protects them from L. monocytogenes-induced death whereas lactoferricin B, its derivative peptide, determines a shifting of the equilibrium from necrosis to apoptosis.

scholarly journals Deciphering the landscape of host barriers to Listeria monocytogenes infection

2017 ◽  
Vol 114 (24) ◽  
pp. 6334-6339 ◽  
Author(s):  
Ting Zhang ◽  
Sören Abel ◽  
Pia Abel zur Wiesch ◽  
Jumpei Sasabe ◽  
Brigid M. Davis ◽  
...  
Keyword(s):  
Population Dynamics ◽  
Listeria Monocytogenes ◽  
Critical Role ◽  
Innate Immune ◽  
Microbial Populations ◽  
Multiple Organs ◽  
Founding Population ◽  
Food Borne ◽  
Listeria Monocytogenes Infection ◽  
The Impact

Listeria monocytogenes is a common food-borne pathogen that can disseminate from the intestine and infect multiple organs. Here, we used sequence tag-based analysis of microbial populations (STAMP) to investigate L. monocytogenes population dynamics during infection. We created a genetically barcoded library of murinized L. monocytogenes and then used deep sequencing to track the pathogen’s dissemination routes and quantify its founding population (Nb) sizes in different organs. We found that the pathogen disseminates from the gastrointestinal tract to distal sites through multiple independent routes and that Nb sizes vary greatly among tissues, indicative of diverse host barriers to infection. Unexpectedly, comparative analyses of sequence tags revealed that fecally excreted organisms are largely derived from the very small number of L. monocytogenes cells that colonize the gallbladder. Immune depletion studies suggest that distinct innate immune cells restrict the pathogen’s capacity to establish replicative niches in the spleen and liver. Finally, studies in germ-free mice suggest that the microbiota plays a critical role in the development of the splenic, but not the hepatic, barriers that prevent L. monocytogenes from seeding these organs. Collectively, these observations illustrate the potency of the STAMP approach to decipher the impact of host factors on population dynamics of pathogens during infection.

scholarly journals Detoxification of methylglyoxal by the glyoxalase system is required for glutathione availability and virulence activation in Listeria monocytogenes

2021 ◽  
Vol 17 (8) ◽  
pp. e1009819
Author(s):  
Andrea Anaya-Sanchez ◽  
Ying Feng ◽  
John C. Berude ◽  
Daniel A. Portnoy
Keyword(s):  
Listeria Monocytogenes ◽  
Transcriptional Activation ◽  
Protein Glycation ◽  
Host Cells ◽  
Intracellular Pathogen ◽  
Cell Monolayers ◽  
Food Borne ◽  
Virulence Regulator ◽  
Allosteric Activator

Listeria monocytogenes is a Gram-positive, food-borne pathogen that lives a biphasic lifestyle, cycling between the environment and as a facultative intracellular pathogen of mammals. Upon entry into host cells, L. monocytogenes upregulates expression of glutathione synthase (GshF) and its product, glutathione (GSH), which is an allosteric activator of the master virulence regulator PrfA. Although gshF mutants are highly attenuated for virulence in mice and form very small plaques in host cell monolayers, these virulence defects can be fully rescued by mutations that lock PrfA in its active conformation, referred to as PrfA*. While PrfA activation can be recapitulated in vitro by the addition of reducing agents, the precise biological cue(s) experienced by L. monocytogenes that lead to PrfA activation are not known. Here we performed a genetic screen to identify additional small-plaque mutants that were rescued by PrfA* and identified gloA, which encodes glyoxalase A, a component of a GSH-dependent methylglyoxal (MG) detoxification system. MG is a toxic byproduct of metabolism produced by both the host and pathogen, which if accumulated, causes DNA damage and protein glycation. As a facultative intracellular pathogen, L. monocytogenes must protect itself from MG produced by its own metabolic processes and that of its host. We report that gloA mutants grow normally in broth, are sensitive to exogenous MG and severely attenuated upon IV infection in mice, but are fully rescued for virulence in a PrfA* background. We demonstrate that transcriptional activation of gshF increased upon MG challenge in vitro, and while this resulted in higher levels of GSH for wild-type L. monocytogenes, the glyoxalase mutants had decreased levels of GSH, presumably due to the accumulation of the GSH-MG hemithioacetal adduct. These data suggest that MG acts as a host cue that leads to GSH production and activation of PrfA.

Anti-Invasive Activity of Bovine Lactoferrin against Listeria monocytogenes

1997 ◽  
Vol 60 (3) ◽  
pp. 267-271 ◽  
Author(s):  
GIOVANNI ANTONINI ◽  
MARIA ROSARIA CATANIA ◽  
RITA GRECO ◽  
CATIA LONGHI ◽  
MARIA GRAZIA PISCIOTTA ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Toxic Effect ◽  
Intestinal Epithelium ◽  
Bacterial Infections ◽  
In Vitro Model ◽  
Bovine Lactoferrin ◽  
Food Borne ◽  
Vitro Model

We have investigated the possible role of bovine lactoferrin in protecting the intestinal epithelium from bacterial infections, using as an in vitro model enterocyte-like cell lines HT-39 and Caco-2 infected with a food-borne pathogen, Listeria monocytogenes. When infection occurred in the presence of 1 mg/ml of bovine lactoferrin, in the form of apolactoferrin or iron- or manganese-saturated forms, the adhesion of bacteria to eukaryotk cells was unaffected, but the number of internalized bacteria was reduced by 42- to 125-fold. The possibility of a toxic effect of lactoferrin was excluded, because bovine lactoferrin was used at nonbactericidal and noncytotoxic concentrations.

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

2018 ◽  
Vol 24 (4) ◽  
pp. 252-261 ◽  
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.

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