CD44-Regulated Intracellular Proliferation of<i>Listeria monocytogenes</i>

Eriksson, Emma; Dons, Lone; Rothfuchs, Antonio Gigliotti; Heldin, Paraskevi; Wigzell, Hans; Rottenberg, Martı́n E.

doi:10.1128/iai.71.7.4102-4111.2003

Cited by 11 publications

(14 citation statements)

References 47 publications

(39 reference statements)

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“…This process requires ezrin phosphorylation and activation, which opens an F-actin binding site on the molecule. CD44 can also block actin polymerization through interactions with merlin, another band 4.1 protein that competes with and displaces ezrin (683,684). Unlike ezrin, merlin lacks an F-actin binding motif and cannot support protrusion formation.…”

Section: Listeriamentioning

confidence: 99%

Blood Groups in Infection and Host Susceptibility

2015

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SUMMARY Blood group antigens represent polymorphic traits inherited among individuals and populations. At present, there are 34 recognized human blood groups and hundreds of individual blood group antigens and alleles. Differences in blood group antigen expression can increase or decrease host susceptibility to many infections. Blood groups can play a direct role in infection by serving as receptors and/or coreceptors for microorganisms, parasites, and viruses. In addition, many blood group antigens facilitate intracellular uptake, signal transduction, or adhesion through the organization of membrane microdomains. Several blood groups can modify the innate immune response to infection. Several distinct phenotypes associated with increased host resistance to malaria are overrepresented in populations living in areas where malaria is endemic, as a result of evolutionary pressures. Microorganisms can also stimulate antibodies against blood group antigens, including ABO, T, and Kell. Finally, there is a symbiotic relationship between blood group expression and maturation of the gastrointestinal microbiome.

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Section: Listeriamentioning

confidence: 99%

Blood Groups in Infection and Host Susceptibility

2015

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“…Primary fibroblast cultures were generated, as described (40). The pulmonary vasculature was perfused, and lungs were aseptically removed, excised into small pieces, and subjected to collagenase digestion at 37°C for 15 min under agitation.…”

Section: Generation Of Fibroblasts From Mouse Lungmentioning

confidence: 99%

Intracellular Bacterial Infection-Induced IFN-γ Is Critically but Not Solely Dependent on Toll-Like Receptor 4-Myeloid Differentiation Factor 88-IFN-αβ-STAT1 Signaling

Rothfuchs

Trumstedt

Wigzell

et al. 2004

The Journal of Immunology

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Infection of murine bone marrow-derived macrophages (BMMφ) with Chlamydia pneumoniae induces IFN-αβ-dependent IFN-γ secretion that leads to control of the intracellular bacterial growth. Enhanced growth of C. pneumoniae in Toll-like receptor (TLR) 4−/− and myeloid differentiation factor (MyD) 88−/− (but not TLR2−/−, TLR6−/−, or TLR9−/−) BMMφ is shown in this study. Reduced accumulation of IFN-α and IFN-γ mRNA was also observed in TLR4−/−- and MyD88−/−-infected cells. IL-1R and IL-18R signaling did not account for differences between MyD88−/− and wild-type BMMφ. Surprisingly, infection-induced NF-κB activation as well as TNF-α, IL-1, or IL-6 mRNA expression were all normal in TLR4−/− and MyD88−/− cells. Phosphorylation of the transcription factor STAT1 during bacterial infection is IFN-αβ dependent, and necessary for increased IFN-γ mRNA accumulation and chlamydial growth control. Signaling through common cytokine receptor γ-chain and RNA-dependent protein kinase both mediated IFN-αβ-dependent enhancement of IFN-γ mRNA levels. Accumulation of IFN-γ mRNA and control of C. pneumoniae growth required NF-κB activation. Such NF-κB activation was independent of IFN-αβ, STAT1, and RNA-dependent protein kinase. In summary, C. pneumoniae-induced IFN-γ expression in BMMφ is controlled by a TLR4-MyD88-IFN-αβ-STAT1-dependent pathway, as well as by a TLR4-independent pathway leading to NF-κB activation.

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“…Plasmid segregation assay. The plasmid pAUL‐A [27], which replicates at 30 °C, but not at 37 °C, and possesses an erythromycin‐resistance gene, was used to distinguish replication rate from death rate of L. monocytogenes as previously described [28]. L. monocytogenes EGD was transformed with pAUL‐A by electroporation and was grown at 30 °C in BHI medium containing 5 µg/ml of erythromycin overnight.…”

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confidence: 99%

Interferon‐γ Mediates Neuronal Killing of Intracellular Bacteria

et al. 2004

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Neurons can be targets for microbes, which could kill the neurons. Just in reverse, we, in this study, report that bacteria can be killed when entering a neuron. Primary cultures of foetal mouse hippocampal neurons and a neuronal cell line derived from mouse hypothalamus were infected by Listeria monocytogenes. Treatment with interferon-g (IFN-g) did not affect bacterial uptake, but resulted in increased killing of intracellular bacteria, whereas the neuronal cell remained intact. The IFN-g-mediated bacterial killing was mapped to the neuronal cytosol, before listerial actin tail formation. Treatment with IFN-g induced phosphorylation of the transcription factor STAT-1 in neurons and IFN-g-mediated listerial killing was not observed in STAT-1 -/-neurons or neurons treated with IFN regulatory factor-1 antisense oligonucleotides. IFN-g-treated neuronal cells showed increased levels of inducible nitric oxide synthase (iNOS) mRNA, and antisense iNOS oligonucleotides hampered the bacterial killing by neurons upon IFN-g treatment. This novel neuronal function -i.e., that of a microbe killer -could play a crucial role in the control of infections in the immuno-privileged nervous system.

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CD44-Regulated Intracellular Proliferation ofListeria monocytogenes

Cited by 11 publications

References 47 publications

Blood Groups in Infection and Host Susceptibility

Blood Groups in Infection and Host Susceptibility

Intracellular Bacterial Infection-Induced IFN-γ Is Critically but Not Solely Dependent on Toll-Like Receptor 4-Myeloid Differentiation Factor 88-IFN-αβ-STAT1 Signaling

Interferon‐γ Mediates Neuronal Killing of Intracellular Bacteria

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