The loss of contact inhibition and anchorage-dependent growth are key steps in the acquisition of Listeria monocytogenes susceptibility phenotype by non-phagocytic cells

1995 ◽  
Vol 85 (1) ◽  
pp. 55-66 ◽  
Author(s):  
Philippe Velge ◽  
Bertrand Kaeffer ◽  
Elisabeth Bottreau ◽  
Nathalie Langendonck
Keyword(s):  
Listeria Monocytogenes ◽  
Contact Inhibition ◽  
Phagocytic Cells ◽  
Loss Of Contact ◽  
Dependent Growth ◽  
Key Steps

scholarly journals Lymphocytes are detrimental during the early innate immune response against Listeria monocytogenes

2006 ◽  
Vol 203 (4) ◽  
pp. 933-940 ◽  
Author(s):  
Javier A. Carrero ◽  
Boris Calderon ◽  
Emil R. Unanue
Keyword(s):  
Immune Response ◽  
Listeria Monocytogenes ◽  
Innate Immune Response ◽  
Early Stage ◽  
Bacterial Pathogen ◽  
Interleukin 10 ◽  
Innate Immune ◽  
Type I ◽  
Phagocytic Cells ◽  
Immunodeficient Mice

Mice deficient in lymphocytes are more resistant than normal mice to Listeria monocytogenes infection during the early innate immune response. This paradox remains unresolved: lymphocytes are required for sterilizing immunity, but their presence during the early stage of the infection is not an asset and may even be detrimental. We found that lymphocyte-deficient mice, which showed limited apoptosis in infected organs, were resistant during the first four days of infection but became susceptible when engrafted with lymphocytes. Engraftment with lymphocytes from type I interferon receptor–deficient (IFN-αβR−/−) mice, which had reduced apoptosis, did not confer increased susceptibility to infection, even when the phagocytes were IFN-αβR+/+. The attenuation of innate immunity was due, in part, to the production of the antiinflammatory cytokine interleukin 10 by phagocytic cells after the apoptotic phase of the infection. Thus, immunodeficient mice were more resistant relative to normal mice because the latter went through a stage of lymphocyte apoptosis that was detrimental to the innate immune response. This is an example of a bacterial pathogen creating a cascade of events that leads to a permissive infective niche early during infection.

Involvement of up-regulated Necl-5/Tage4/PVR/CD155 in the loss of contact inhibition in transformed NIH3T3 cells

2007 ◽  
Vol 352 (4) ◽  
pp. 856-860 ◽  
Author(s):  
Yukiko Minami ◽  
Wataru Ikeda ◽  
Mihoko Kajita ◽  
Tsutomu Fujito ◽  
Morito Monden ◽  
...  
Keyword(s):  
Contact Inhibition ◽  
Nih3t3 Cells ◽  
Loss Of Contact

Depletion of GRIM-19 accelerates hepatocellular carcinoma invasion via inducing EMT and loss of contact inhibition

2011 ◽  
Vol 227 (3) ◽  
pp. 1212-1219 ◽  
Author(s):  
Hongbo Hao ◽  
Jun Liu ◽  
Guoliang Liu ◽  
Dongshi Guan ◽  
Yang Yang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Contact Inhibition ◽  
Loss Of Contact

scholarly journals σ B contributes to Listeria monocytogenes invasion by controlling expression of inlA and inlB

Microbiology ◽  
2005 ◽  
Vol 151 (10) ◽  
pp. 3215-3222 ◽  
Author(s):  
Heesun Kim ◽  
Hélène Marquis ◽  
Kathryn J. Boor
Keyword(s):  
Listeria Monocytogenes ◽  
Stationary Phase ◽  
Critical Role ◽  
Virulence Gene ◽  
Bacterial Invasion ◽  
Dependent Manner ◽  
Intestinal Epithelial ◽  
Phagocytic Cells ◽  
Invasion Mechanisms ◽  
Human Enterocyte

The ability of Listeria monocytogenes to invade non-phagocytic cells is important for development of a systemic listeriosis infection. The authors previously reported that a L. monocytogenes ΔsigB strain is defective in invasion into human intestinal epithelial cells, in part, due to decreased expression of a major invasion gene, inlA. To characterize additional invasion mechanisms under the control of σ B, mutants were generated carrying combinations of in-frame deletions in inlA, inlB and sigB. Quantitative assessment of bacterial invasion into the human enterocyte Caco-2 and hepatocyte HepG-2 cell lines demonstrated that σ B contributes to both InlA and InlB-mediated invasion of L. monocytogenes. Previous identification of the σ B-dependent P2 prfA promoter upstream of the major virulence gene regulator, positive regulatory factor A (PrfA), suggested that the contributions of σ B to expression of various virulence genes, including inlA, could be at least partially mediated through PrfA. To test this hypothesis, relative invasion capabilities of ΔsigB and ΔprfA strains were compared. Exponential-phase cells of the ΔsigB and ΔprfA strains were similarly defective at invasion; however, stationary-phase ΔsigB cells were significantly less invasive than stationary-phase ΔprfA cells, suggesting that the contributions of σ B to invasion extend beyond those mediated through PrfA in stationary-phase L. monocytogenes. TaqMan quantitative reverse-transcriptase PCRs further demonstrated that expression of inlA and inlB was greatly increased in a σ B-dependent manner in stationary-phase L. monocytogenes. Together, results from this study provide strong biological evidence of a critical role for σ B in L. monocytogenes invasion into non-phagocytic cells, primarily mediated through control of inlA and inlB expression.

scholarly journals Conditional Lethality Yields a New Vaccine Strain of Listeria monocytogenes for the Induction of Cell-Mediated Immunity

2005 ◽  
Vol 73 (8) ◽  
pp. 5065-5073 ◽  
Author(s):  
Zhongxia Li ◽  
Xinyan Zhao ◽  
Darren E. Higgins ◽  
Fred R. Frankel
Keyword(s):  
Listeria Monocytogenes ◽  
Inducible Promoter ◽  
Vector System ◽  
Cell Mediated Immunity ◽  
Multicopy Plasmid ◽  
Listeriolysin O ◽  
Delivery Vector ◽  
Immunodeficiency Virus ◽  
Dependent Growth

ABSTRACT Listeria monocytogenes is a gram-positive intracellular pathogen that can enter phagocytic and nonphagocytic cells and colonize their cytosols. Taking advantage of this property to generate an intracellular vaccine delivery vector, we previously described a mutant strain of L. monocytogenes, Δdal Δdat, which is unable to synthesize cell wall by virtue of deletions in two genes (dal and dat) required for d-alanine synthesis. This highly attenuated strain induced long-lived protective systemic and mucosal immune responses in mice when administered in the transient presence of d-alanine. We have now increased the usefulness of this organism as a vaccine vector by use of an inducible complementation system that obviates the need for exogenous d-alanine administration. The strain expresses a copy of the Bacillus subtilis racemase gene under the control of a tightly regulated isopropyl-β-d-thiogalactopyranoside (IPTG)-inducible promoter present on a multicopy plasmid. This bacterium demonstrates strict dose-dependent growth in the presence of IPTG. After removal of inducer, bacterial growth ceased within two replication cycles. Following infection of mice in the absence of IPTG or d-alanine, the bacterium survived in vivo for less than 3 days. Nevertheless, a single immunization elicited a state of long-lasting protective immunity against wild-type L. monocytogenes and induced a subset of effector listeriolysin O-specific CD11a+ CD8+ T cells in spleen and other tissues that was strongly enhanced after secondary immunization. This improved L. monocytogenes vector system may have potential use as a live vaccine against human immunodeficiency virus, other infectious diseases, and cancer.

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