CD8+ T-cell-mediated response to Listeria monocytogenes taken up in the liver and replicating within hepatocytes

Gregory, Stephen H.; Liu, Chau‐Ching

doi:10.1034/j.1600-0528.2002.017405.x

Cited by 28 publications

(26 citation statements)

References 96 publications

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“…However, the liver is the site of replication of many bacterial pathogens for which multiplication in an intracellular compartment is an integral element of pathogenesis. For example, Listeria monocytogenes invades hepatocytes following uptake by liver macrophages, and intracellular multiplication induces the hepatocytes to undergo apoptosis, resulting in the release of interleukin-1␣ and an innate immune response leading to microabscess formation (28,29,56). However, the formation of abscesses was not observed in livers of S. iniae-infected zebrafish.…”

Section: Discussionmentioning

confidence: 99%

Streptococcus-Zebrafish Model of Bacterial Pathogenesis

Neely¹,

Pfeifer

Caparon³

2002

Infect Immun

301

286

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Due to its small size, rapid generation time, powerful genetic systems, and genomic resources, the zebrafish has emerged as an important model of vertebrate development and human disease. Its well-developed adaptive and innate cellular immune systems make the zebrafish an ideal model for the study of infectious diseases. With a natural and important pathogen of fish, Streptococcus iniae, we have established a streptococcuszebrafish model of bacterial pathogenesis. Following injection into the dorsal muscle, zebrafish developed a lethal infection, with a 50% lethal dose of 10 3 CFU, and died within 2 to 3 days. The pathogenesis of infection resembled that of S. iniae in farmed fish populations and that of several important human streptococcal diseases and was characterized by an initial focal necrotic lesion that rapidly progressed to invasion of the pathogen into all major organ systems, including the brain. Zebrafish were also susceptible to infection by the human pathogen Streptococcus pyogenes. However, disease was characterized by a marked absence of inflammation, large numbers of extracellular streptococci in the dorsal muscle, and extensive myonecrosis that occurred far in advance of any systemic invasion. The genetic systems available for streptococci, including a novel method of mutagenesis which targets genes whose products are exported, were used to identify several mutants attenuated for virulence in zebrafish. This combination of a genetically amenable pathogen with a well-defined vertebrate host makes the streptococcus-zebrafish model of bacterial pathogenesis a powerful model for analysis of infectious disease.

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Section: Discussionmentioning

confidence: 99%

Streptococcus-Zebrafish Model of Bacterial Pathogenesis

Neely¹,

Pfeifer

Caparon³

2002

Infect Immun

301

286

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“…L. monocytogenes is capable of persistent intracellular survival and replication in epithelial cells, endothelial cells, dendritic cells, fibroblasts, and macrophages [317]. Hepatocytes represent the principle site for intracellular replication [319], although macrophages may also be an important reservoir [320]. In fact, L. monocytogenes can completely avoid the extracellular environment within the host by moving from cell to cell via polarized actin polymerization-dependent mechanisms [316,317,321].…”

Section: Streptococcus Sppmentioning

confidence: 99%

“…Second, PCD would expose the bacteria to the extracellular milieu, where they are susceptible to extracellular effectors of immunity [319,335]. Neutrophils may mediate hepatocyte death and abort the cycle of cell-tocell spread [13,326,336], though PCD may also occur in hepatocytes in the absence of neutrophils [328,337].…”

Section: Streptococcus Sppmentioning

confidence: 99%

Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity

Ulett

Adderson²

2006

CIR

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Apoptosis, or programmed cell death (PCD), is an important physiological mechanism, through which the human immune system regulates homeostasis and responds to diverse forms of cellular damage. PCD may also be involved in immune counteraction to microbial infection. Over the past decade, the amount of research on bacteria-induced PCD has grown tremendously, and the implications of this mechanism on immunity are being elucidated. Some pathogenic bacteria actively trigger the suicide response in critical lineages of leukocytes that orchestrate both the innate and adaptive immune responses; other bacteria proactively prevent PCD to benefit their own survival and persistence. Currently, the microbial virulence factors, which represent the keys to unlocking the suicide response in host cells, are a primary focus of this field. In this review, we discuss these bacterial "apoptosis regulatory molecules" and the apoptotic events they either trigger or prevent, the host target cells of this regulatory activity, and the possible ramifications for immunity to infection. Gram-positive pathogens including Staphylococcus, Streptococcus, Bacillus, Listeria, and Clostridia species are discussed as important agents of human infection that modulate PCD pathways in eukaryotic cells.

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“…The harmless Ag from dietary proteins and commensal microflora is generally met with immune tolerance in this organ (1). In contrast, liver-trophic pathogens provoke innate and adaptive immune reactions (2). Liver grafts of many species are frequently accepted by their MHC-incompatible hosts and promote tolerance to additional donor organs transplanted along with the liver (3).…”

mentioning

confidence: 99%

Hepatocytes Express Abundant Surface Class I MHC and Efficiently Use Transporter Associated with Antigen Processing, Tapasin, and Low Molecular Weight Polypeptide Proteasome Subunit Components of Antigen Processing and Presentation Pathway

Chen

Tabaczewski

Truscott

et al. 2005

The Journal of Immunology

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Hepatic expression levels of class I MHC Ags are generally regarded as very low. Because the status of these Ags and their ability to present peptides are important for the understanding of pathogen clearance and tolerogenic properties of the liver, we set out to identify the factors contributing to the reported phenotype. Unexpectedly, we found that the surface densities of Kb and Db on C57BL/6 mouse hepatocytes are nearly as high as on splenocytes, as are the lysate concentrations of mRNA encoding H chain and β2-microglobulin (β2m). In contrast, the components of the peptide-loading pathway are reduced in hepatocytes. Despite the difference in the stoichiometric ratios of H chain/β2m/peptide-loading machineries, both cell types express predominantly thermostable class I and are critically dependent on TAP and tapasin for display of surface Ags. Minor differences in the expression patterns in tapasin−/− background suggest cell specificity in class I assembly. Under immunostimulatory conditions, such as exposure to IFN-γ or Listeria monocytogenes, hepatocytes respond with a vigorous mRNA synthesis of the components of the Ag presentation pathway (up to 10-fold enhancement) but up-regulate H chain and β2m to a lesser degree (<2-fold). This type of response should promote rapid influx of newly generated peptides into the endoplasmic reticulum and preferential presentation of foreign/induced Ag by hepatic class I.

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CD8+ T-cell-mediated response to Listeria monocytogenes taken up in the liver and replicating within hepatocytes

Cited by 28 publications

References 96 publications

Streptococcus-Zebrafish Model of Bacterial Pathogenesis

Streptococcus-Zebrafish Model of Bacterial Pathogenesis

Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity

Hepatocytes Express Abundant Surface Class I MHC and Efficiently Use Transporter Associated with Antigen Processing, Tapasin, and Low Molecular Weight Polypeptide Proteasome Subunit Components of Antigen Processing and Presentation Pathway

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