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Restricted replication of Listeria monocytogenes in a gamma interferon-activated murine hepatocyte line.
Infect Immun. 1995 Aug; 63(8):3187-95.II

Abstract

The intracellular pathogen Listeria monocytogenes replicates mainly in resting macrophages and hepatocytes residing in infected tissues. Both innate and acquired resistance strongly depend on activation of listericidal capacities of macrophages by gamma interferon (IFN-gamma) produced by natural killer cells and T lymphocytes. In contrast to macrophages, hepatocytes have been considered to serve purely as a cellular habitat, prolonging survival of the pathogen in the host. By using an immortalized murine hepatocyte line, the relationship between L. monocytogenes and this cell type has been analyzed in more detail. Our data reveal that hepatocytes are able to eradicate listeriolysin-deficient (avirulent) L. monocytogenes but fail to control growth of listeriolysin-expressing (virulent) L. monocytogenes organisms. Following stimulation with IFN-gamma, hepatocytes gained the capacity to restrict growth of virulent L. monocytogenes, although less efficiently than the highly listericidal IFN-gamma-activated macrophages. Hepatocytes costimulated with a combination of IFN-gamma, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) expressed the highest antilisterial activities. Although IFN-gamma-stimulated hepatocytes produced demonstrable levels of reactive nitrogen intermediates (RNI), the results of inhibition studies do not support a major role for these molecules in antilisterial hepatocyte activities. In contrast, inhibition of RNI produced by macrophages neutralized their antilisterial effects. IFN-gamma-stimulated, L. monocytogenes-infected hepatocytes expressed TNF-alpha mRNA, suggesting that they are a source of this cytokine during listeriosis. These studies suggest a novel function for hepatocytes in listeriosis: first, IFN-gamma-stimulated hepatocytes could contribute to listerial growth restriction in the liver, and second, through secretion of proinflammatory cytokines, they could promote phagocyte influx to the site of listerial growth.

Authors+Show Affiliations

Department of Immunology, University of Ulm, Germany.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

7542640

Citation

Szalay, G, et al. "Restricted Replication of Listeria Monocytogenes in a Gamma Interferon-activated Murine Hepatocyte Line." Infection and Immunity, vol. 63, no. 8, 1995, pp. 3187-95.
Szalay G, Hess J, Kaufmann SH. Restricted replication of Listeria monocytogenes in a gamma interferon-activated murine hepatocyte line. Infect Immun. 1995;63(8):3187-95.
Szalay, G., Hess, J., & Kaufmann, S. H. (1995). Restricted replication of Listeria monocytogenes in a gamma interferon-activated murine hepatocyte line. Infection and Immunity, 63(8), 3187-95.
Szalay G, Hess J, Kaufmann SH. Restricted Replication of Listeria Monocytogenes in a Gamma Interferon-activated Murine Hepatocyte Line. Infect Immun. 1995;63(8):3187-95. PubMed PMID: 7542640.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Restricted replication of Listeria monocytogenes in a gamma interferon-activated murine hepatocyte line. AU - Szalay,G, AU - Hess,J, AU - Kaufmann,S H, PY - 1995/8/1/pubmed PY - 1995/8/1/medline PY - 1995/8/1/entrez SP - 3187 EP - 95 JF - Infection and immunity JO - Infect. Immun. VL - 63 IS - 8 N2 - The intracellular pathogen Listeria monocytogenes replicates mainly in resting macrophages and hepatocytes residing in infected tissues. Both innate and acquired resistance strongly depend on activation of listericidal capacities of macrophages by gamma interferon (IFN-gamma) produced by natural killer cells and T lymphocytes. In contrast to macrophages, hepatocytes have been considered to serve purely as a cellular habitat, prolonging survival of the pathogen in the host. By using an immortalized murine hepatocyte line, the relationship between L. monocytogenes and this cell type has been analyzed in more detail. Our data reveal that hepatocytes are able to eradicate listeriolysin-deficient (avirulent) L. monocytogenes but fail to control growth of listeriolysin-expressing (virulent) L. monocytogenes organisms. Following stimulation with IFN-gamma, hepatocytes gained the capacity to restrict growth of virulent L. monocytogenes, although less efficiently than the highly listericidal IFN-gamma-activated macrophages. Hepatocytes costimulated with a combination of IFN-gamma, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) expressed the highest antilisterial activities. Although IFN-gamma-stimulated hepatocytes produced demonstrable levels of reactive nitrogen intermediates (RNI), the results of inhibition studies do not support a major role for these molecules in antilisterial hepatocyte activities. In contrast, inhibition of RNI produced by macrophages neutralized their antilisterial effects. IFN-gamma-stimulated, L. monocytogenes-infected hepatocytes expressed TNF-alpha mRNA, suggesting that they are a source of this cytokine during listeriosis. These studies suggest a novel function for hepatocytes in listeriosis: first, IFN-gamma-stimulated hepatocytes could contribute to listerial growth restriction in the liver, and second, through secretion of proinflammatory cytokines, they could promote phagocyte influx to the site of listerial growth. SN - 0019-9567 UR - https://www.unboundmedicine.com/medline/citation/7542640/Restricted_replication_of_Listeria_monocytogenes_in_a_gamma_interferon_activated_murine_hepatocyte_line_ L2 - http://iai.asm.org/cgi/pmidlookup?view=long&pmid=7542640 DB - PRIME DP - Unbound Medicine ER -