Innate defenses in the liver during Listeria infection

Cousens, Leslie P.; Wing, Edward J.

doi:10.1034/j.1600-0528.2002.017407.x

Cited by 94 publications

(73 citation statements)

References 89 publications

(133 reference statements)

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“…3 is a Gram-positive facultative intracellular bacterium that often causes life-threatening infections in an immunocompromised host, including newborns and elderly people (1)(2)(3). In host liver, LM invades and replicates in hepatocytes and Kupffer cells, tissue macrophages (2).…”

Section: Isteria Monocytogenes (Lm)mentioning

confidence: 99%

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Critical Roles of Myeloid Differentiation Factor 88-Dependent Proinflammatory Cytokine Release in Early Phase Clearance ofListeria monocytogenesin Mice

Seki

Tsutsui

Tsuji

et al. 2002

The Journal of Immunology

254

203

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Listeria monocytogenes (LM), a facultative intracellular Gram-positive bacterium, often causes lethal infection of the host. In this study we investigated the molecular mechanism underlying LM eradication in the early phase of infection. Upon infection with LM, both IL-12 and IL-18 were produced, and then they synergistically induced IFN-γ production, leading to normal LM clearance in the host. IFN-γ knockout (KO) mice were highly susceptible to LM infection. IL-12/IL-18 double knockout mice were also highly susceptible. Their susceptibility was less than that of IFN-γ KO mice, but more than that of single IL-12 or IL-18 KO mice. Mice deficient in myeloid differentiation factor 88 (MyD88), an essential adaptor molecule used by signal transduction pathways of all members of the Toll-like receptor (TLR) family, showed an inability to produce IL-12 and IFN-γ following LM infection and were most susceptible to LM. Furthermore, MyD88-deficient, but not IFN-γ-deficient, Kupffer cells could not produce TNF-α in response to LM in vitro, indicating the importance of MyD88-dependent TNF-α production for host defense. As TLR2 KO, but not TLR4 KO, mice showed partial impairment in their capacity to produce IL-12, IFN-γ, and TNF-α, TLR2 activation partly contributed to the induction of IL-12-mediated IFN-γ production. These results indicated a critical role for TLRs/MyD88-dependent IL-12/TNF-α production and for IL-12- and IL-18-mediated IFN-γ production in early phase clearance of LM.

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Section: Isteria Monocytogenes (Lm)mentioning

confidence: 99%

“…In host liver, LM invades and replicates in hepatocytes and Kupffer cells, tissue macrophages (2). The activation of the host's innate immune system is critical for LM eradication in the early phase of infection (2)(3)(4).…”

Section: Isteria Monocytogenes (Lm)mentioning

confidence: 99%

Critical Roles of Myeloid Differentiation Factor 88-Dependent Proinflammatory Cytokine Release in Early Phase Clearance ofListeria monocytogenesin Mice

Seki

Tsutsui

Tsuji

et al. 2002

The Journal of Immunology

254

203

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show abstract

“…This either eliminates the microbe or modifies bacterial expansion, thereby preventing overwhelming sepsis. At the same time, the stage is set for T cell-dependent elimination of the pathogen (Cousens and Wing, 2000;Pamer, 2004). The significance of innate immune responses during listeriosis is emphasized by the fact that scid mice, i.e.…”

Section: Introductionmentioning

confidence: 99%

Mast cells initiate early anti-Listeria host defences

Gekara¹,

Weiß²

2007

Cell Microbiol

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“…Mouse studies typically employ intravenous injection of Listeria, which results in systemic infection 2 . After injection, Listeria quickly disseminates to the spleen and liver due to uptake by CD8α + dendritic cells and Kupffer cells 3,4 . .…”

Section: Introductionmentioning

confidence: 99%

“…After injection, Listeria quickly disseminates to the spleen and liver due to uptake by CD8α + dendritic cells and Kupffer cells 3,4 . Once phagocytosed, various bacterial proteins enable Listeria to escape the phagosome, survive within the cytosol, and infect neighboring cells 5 .…”

mentioning

confidence: 99%

Measuring Bacterial Load and Immune Responses in Mice Infected with <em>Listeria monocytogenes</em>

Wang

Strugnell

Wijburg

et al. 2011

JoVE

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Listeria monocytogenes (Listeria) is a Gram-positive facultative intracellular pathogen 1 . Mouse studies typically employ intravenous injection of Listeria, which results in systemic infection 2 . After injection, Listeria quickly disseminates to the spleen and liver due to uptake by CD8α + dendritic cells and Kupffer cells 3,4 . . Generally, mice with increased susceptibility to Listeria infection are less able to control bacterial proliferation, demonstrating increased bacterial load and/or delayed clearance compared to resistant mice. Genetic studies, including linkage analyses and knockout mouse strains, have identified various genes for which sequence variation affects host responses to Listeria infection 6,[8][9][10][11][12][13][14] . Determination and comparison of infection kinetics between different mouse strains is therefore an important method for identifying host genetic factors that contribute to immune responses against Listeria. Comparison of host responses to different Listeria strains is also an effective way to identify bacterial virulence factors that may serve as potential targets for antibiotic therapy or vaccine design.We describe here a straightforward method for measuring bacterial load (colony forming units [CFU] per tissue) and preparing single-cell suspensions of the liver and spleen for FACS analysis of immune responses in Listeria-infected mice. This method is particularly useful for initial characterization of Listeria infection in novel mouse strains, as well as comparison of immune responses between different mouse strains infected with Listeria. We use the Listeria monocytogenes EGD strain 15 that, when cultured on blood agar, exhibits a characteristic halo zone around each colony due to β-hemolysis 1 (Figure 1). Bacterial load and immune responses can be determined at any time-point after infection by culturing tissue homogenate on blood agar plates and preparing tissue cell suspensions for FACS analysis using the protocols described below. We would note that individuals who are immunocompromised or pregnant should not handle Listeria, and the relevant institutional biosafety committee and animal facility management should be consulted before work commences. Video LinkThe video component of this article can be found at https://www.jove.com/video/3076/ Protocol 1. Culturing and long-term storage of Listeria monocytogenes (Listeria)1. Make or purchase pre-made horse blood agar (HBA) plates. Dry plates prior to use by pre-incubating at 37°C overnight or placing uncovered in a laminar flow cabinet for 1 hour. 2. Obtain viable Listeria from one of the following: an infected mouse tissue homogenate, a lyophilized stock, a frozen glycerol stock, or a colony from a recent Listeria culture (i.e. less than one-week old and not sub-cultured more than 10 generations). All Listeria should be obtained using a sterile inoculating loop and employing aseptic techniques for all methods described in this protocol. 3. Streak Listeria on a HBA plate as shown in Figure 1 using a sterile ino...

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Innate defenses in the liver during Listeria infection

Cited by 94 publications

References 89 publications

Critical Roles of Myeloid Differentiation Factor 88-Dependent Proinflammatory Cytokine Release in Early Phase Clearance ofListeria monocytogenesin Mice

Critical Roles of Myeloid Differentiation Factor 88-Dependent Proinflammatory Cytokine Release in Early Phase Clearance ofListeria monocytogenesin Mice

Mast cells initiate early anti-Listeria host defences

Measuring Bacterial Load and Immune Responses in Mice Infected with <em>Listeria monocytogenes</em>

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