<i>Listeria monocytogenes</i>induces host DNA damage and delays the host cell cycle to promote infection

Leitão, Elsa; Costa, Ana; Brito, Cláudia; Costa, Lionel; Pombinho, Rita; Cabanes, Didier; Sousa, Sandra

doi:10.4161/cc.27780

Cited by 29 publications

(31 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This bacterium, an intracellular facultative pathogen present in contaminated food, is able to cross both the intestine and placenta barriers and spread from cell to cell. It has been shown that L. monocytogenes induces DSBs and γ H2AX at very low MOI (less than 1 bacterium per cell) [64]. This process is independent on the toxin lysteriolysin O (LLO), a pore-forming toxin with cytolytic activity localized at the plasma membrane [64], and bacterial internalization is not necessary for inducing host cell DNA damage [65].…”

Section: Strains Of Shigella Neisseria Listeria and Chlamydia Are Amentioning

confidence: 99%

“…It has been shown that L. monocytogenes induces DSBs and γ H2AX at very low MOI (less than 1 bacterium per cell) [64]. This process is independent on the toxin lysteriolysin O (LLO), a pore-forming toxin with cytolytic activity localized at the plasma membrane [64], and bacterial internalization is not necessary for inducing host cell DNA damage [65]. Infection with L. monocytogenes increases host cell cycle duration without compromising cell viability and infected cells continue division to generate two infected cells [64].…”

Section: Strains Of Shigella Neisseria Listeria and Chlamydia Are Amentioning

confidence: 99%

“…This process is independent on the toxin lysteriolysin O (LLO), a pore-forming toxin with cytolytic activity localized at the plasma membrane [64], and bacterial internalization is not necessary for inducing host cell DNA damage [65]. Infection with L. monocytogenes increases host cell cycle duration without compromising cell viability and infected cells continue division to generate two infected cells [64]. In contrast to other bacteria that halt the cell cycle, L. monocytogenes only induces a delay in the DNA synthesis phase, facilitating DNA repair.…”

Section: Strains Of Shigella Neisseria Listeria and Chlamydia Are Amentioning

confidence: 99%

“…This time frame has also been suggested as an auspicious opportunity for the duplication of L. monocytogenes, taking advantage of the host resources for bacterial division. The host DNA damage response (DDR) induced by L. monocytogenes is atypical, as DNA-PK kinase is activated rather than the related kinases ATM or ATR [64]. L. monocytogenes does not possess any known toxin for damaging DNA.…”

Section: Strains Of Shigella Neisseria Listeria and Chlamydia Are Amentioning

confidence: 99%

See 3 more Smart Citations

When our genome is targeted by pathogenic bacteria

Lemercier

2015

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Eukaryotic cells repair thousands of lesions arising in the genome at each cell cycle. The most hazardous damage is likely DNA doublestrand breaks (DSB) that cleave the double helix backbone. DSBs occur naturally during T-cell receptor and immunoglobulin gene recombination in lymphocytes. DSBs can also arise as a consequence of exogenous stresses (e.g. ionizing irradiation, chemotherapeutic drugs, viruses) or oxidative processes. An increasing number of studies have reported that infection with pathogenic bacteria also alters the host genome, producing DSB and other modifications on DNA. This review focuses on recent data on bacteria-induced DNA damage and the known strategies used by these pathogens to maintain a physiological niche in the host. Even after DNA repair in infected cells, "scars" often remain on chromosomes and might generate genomic instability at the next cell division. Chronic inflammation in tissue, combined with infection and DNA damage, can give rise to genomic instability and eventually cancer. A functional link between the DNA damage response and the innate immune response has been recently established. Pathogenic bacteria also highjack the host cell cycle, often acting on the stability of the master regulator p53, or dampen the DNA damage response to support bacterial replication in an appropriate reservoir. Except in a few cases, the molecular mechanisms responsible for DNA lesions are poorly understood, although ROS release during infection is a serious candidate for generating DNA breaks. Thus, chronic or repetitive infections with genotoxic bacteria represent a common source of DNA lesions that compromise host genome integrity.

show abstract

Section: Strains Of Shigella Neisseria Listeria and Chlamydia Are Amentioning

confidence: 99%

Section: Strains Of Shigella Neisseria Listeria and Chlamydia Are Amentioning

confidence: 99%

Section: Strains Of Shigella Neisseria Listeria and Chlamydia Are Amentioning

confidence: 99%

Section: Strains Of Shigella Neisseria Listeria and Chlamydia Are Amentioning

confidence: 99%

See 2 more Smart Citations

When our genome is targeted by pathogenic bacteria

Lemercier

2015

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

show abstract

“…Cette fenêtre temporelle constituerait un créneau propice à la réplication de la bactérie, qui exploite les ressources cellulaires pour se multiplier. La réponse aux dommages provoqués par L. monocytogenes semble atypique puisqu'elle induit de préférence l'activation de la kinase DNA-PK (DNA protein kinase), plutôt que celle de ses protéines apparentées ATM ou ATR (ataxia telangiectasia and Rad3-related protein) [31]. L. monocytogenes ne possède pas de toxine connue pour directement attaquer l'ADN.…”

Section: Identification D'un Nombre Croissant De Bactéries Génotoxiquesunclassified

Les infections bactériennes vues du génome eucaryote

Lemercier

2014

Med Sci (Paris)

View full text Add to dashboard Cite

Proteomics reveals the potential mechanism of Mrps35 controlling Listeria monocytogenes intracellular proliferation in macrophages

Yuan

et al. 2021

Proteomics

View full text Add to dashboard Cite

Macrophages are sentinels in the organism which can resist and destroy various bacteria through direct phagocytosis. Here, we reported that expression level of mitochondrial ribosomal protein S35 (Mrps35) continued to decrease over infection time after Listeria monocytogenes (L. monocytogenes) infected macrophages. Our results indicated that knockdown Mrps35 increased the load of L. monocytogenes in macrophages. This result supported that Mrps35 played the crucial roles in L. monocytogenes infection. Moreover, we performed the comprehensive proteomics to analyze the differentially expressed protein of wild type and Mrps35 Knockdown Raw264.7 cells by L. monocytogenes infection over 6 h. Based on the results of mass spectrometry, we presented a wide variety of hypotheses about the mechanism of Mrps35 controlling the L. monocytogenes intracellular proliferation. Among them, experiments confirmed that Mrps35 and 60S ribosomal protein L22‐like 1 (Rpl22l1) were a functional correlation or potentially a compensatory mechanism during L. monocytogenes infection. This study provided new insights into understanding that L. monocytogenes infection changed the basic synthesis or metabolism‐related proteins of host cells.

show abstract

Listeria monocytogenesinduces host DNA damage and delays the host cell cycle to promote infection

Abstract: (2014) Listeria monocytogenes induces host DNA damage and delays the host cell cycle to promote infection, Cell Cycle, 13:6, 928-940,

Cited by 29 publications

References 46 publications

When our genome is targeted by pathogenic bacteria

When our genome is targeted by pathogenic bacteria

Les infections bactériennes vues du génome eucaryote

Proteomics reveals the potential mechanism of Mrps35 controlling Listeria monocytogenes intracellular proliferation in macrophages

Contact Info

Product

Resources

About