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TNFα-mediated liver destruction by Kupffer cells and Ly6Chi monocytes during Entamoeba histolytica infection

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TNFα-mediated liver destruction by Kupffer cells and Ly6Chi monocytes during Entamoeba histolytica infection. / Helk, Elena; Bernin, Hannah; Ernst, Thomas; Ittrich, Harald; Jacobs, Thomas; Heeren, Joerg; Tacke, Frank; Tannich, Egbert; Lotter, Hannelore.

In: PLOS PATHOG, Vol. 9, No. 1, 01.01.2013, p. e1003096.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Helk, E, Bernin, H, Ernst, T, Ittrich, H, Jacobs, T, Heeren, J, Tacke, F, Tannich, E & Lotter, H 2013, 'TNFα-mediated liver destruction by Kupffer cells and Ly6Chi monocytes during Entamoeba histolytica infection', PLOS PATHOG, vol. 9, no. 1, pp. e1003096. https://doi.org/10.1371/journal.ppat.1003096

APA

Helk, E., Bernin, H., Ernst, T., Ittrich, H., Jacobs, T., Heeren, J., Tacke, F., Tannich, E., & Lotter, H. (2013). TNFα-mediated liver destruction by Kupffer cells and Ly6Chi monocytes during Entamoeba histolytica infection. PLOS PATHOG, 9(1), e1003096. https://doi.org/10.1371/journal.ppat.1003096

Vancouver

Helk E, Bernin H, Ernst T, Ittrich H, Jacobs T, Heeren J et al. TNFα-mediated liver destruction by Kupffer cells and Ly6Chi monocytes during Entamoeba histolytica infection. PLOS PATHOG. 2013 Jan 1;9(1):e1003096. https://doi.org/10.1371/journal.ppat.1003096

Bibtex

@article{e99f4c95b5c643ad90bedd12bb572ba8,
title = "TNFα-mediated liver destruction by Kupffer cells and Ly6Chi monocytes during Entamoeba histolytica infection",
abstract = "Amebic liver abscess (ALA) is a focal destruction of liver tissue due to infection by the protozoan parasite Entamoeba histolytica (E. histolytica). Host tissue damage is attributed mainly to parasite pathogenicity factors, but massive early accumulation of mononuclear cells, including neutrophils, inflammatory monocytes and macrophages, at the site of infection raises the question of whether these cells also contribute to tissue damage. Using highly selective depletion strategies and cell-specific knockout mice, the relative contribution of innate immune cell populations to liver destruction during amebic infection was investigated. Neutrophils were not required for amebic infection nor did they appear to be substantially involved in tissue damage. In contrast, Kupffer cells and inflammatory monocytes contributed substantially to liver destruction during ALA, and tissue damage was mediated primarily by TNFα. These data indicate that besides direct antiparasitic drugs, modulating innate immune responses may potentially be beneficial in limiting ALA pathogenesis.",
keywords = "Animals, Antigens, Ly, Entamoeba histolytica, Entamoebiasis, Immunity, Innate, Inflammation, Kupffer Cells, Liver, Liver Abscess, Amebic, Macrophages, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Monocytes, Neutrophils, Nitric Oxide, Nitric Oxide Synthase Type II, Tumor Necrosis Factor-alpha, omega-N-Methylarginine",
author = "Elena Helk and Hannah Bernin and Thomas Ernst and Harald Ittrich and Thomas Jacobs and Joerg Heeren and Frank Tacke and Egbert Tannich and Hannelore Lotter",
year = "2013",
month = jan,
day = "1",
doi = "10.1371/journal.ppat.1003096",
language = "English",
volume = "9",
pages = "e1003096",
journal = "PLOS PATHOG",
issn = "1553-7366",
publisher = "Public Library of Science",
number = "1",

}

RIS

TY - JOUR

T1 - TNFα-mediated liver destruction by Kupffer cells and Ly6Chi monocytes during Entamoeba histolytica infection

AU - Helk, Elena

AU - Bernin, Hannah

AU - Ernst, Thomas

AU - Ittrich, Harald

AU - Jacobs, Thomas

AU - Heeren, Joerg

AU - Tacke, Frank

AU - Tannich, Egbert

AU - Lotter, Hannelore

PY - 2013/1/1

Y1 - 2013/1/1

N2 - Amebic liver abscess (ALA) is a focal destruction of liver tissue due to infection by the protozoan parasite Entamoeba histolytica (E. histolytica). Host tissue damage is attributed mainly to parasite pathogenicity factors, but massive early accumulation of mononuclear cells, including neutrophils, inflammatory monocytes and macrophages, at the site of infection raises the question of whether these cells also contribute to tissue damage. Using highly selective depletion strategies and cell-specific knockout mice, the relative contribution of innate immune cell populations to liver destruction during amebic infection was investigated. Neutrophils were not required for amebic infection nor did they appear to be substantially involved in tissue damage. In contrast, Kupffer cells and inflammatory monocytes contributed substantially to liver destruction during ALA, and tissue damage was mediated primarily by TNFα. These data indicate that besides direct antiparasitic drugs, modulating innate immune responses may potentially be beneficial in limiting ALA pathogenesis.

AB - Amebic liver abscess (ALA) is a focal destruction of liver tissue due to infection by the protozoan parasite Entamoeba histolytica (E. histolytica). Host tissue damage is attributed mainly to parasite pathogenicity factors, but massive early accumulation of mononuclear cells, including neutrophils, inflammatory monocytes and macrophages, at the site of infection raises the question of whether these cells also contribute to tissue damage. Using highly selective depletion strategies and cell-specific knockout mice, the relative contribution of innate immune cell populations to liver destruction during amebic infection was investigated. Neutrophils were not required for amebic infection nor did they appear to be substantially involved in tissue damage. In contrast, Kupffer cells and inflammatory monocytes contributed substantially to liver destruction during ALA, and tissue damage was mediated primarily by TNFα. These data indicate that besides direct antiparasitic drugs, modulating innate immune responses may potentially be beneficial in limiting ALA pathogenesis.

KW - Animals

KW - Antigens, Ly

KW - Entamoeba histolytica

KW - Entamoebiasis

KW - Immunity, Innate

KW - Inflammation

KW - Kupffer Cells

KW - Liver

KW - Liver Abscess, Amebic

KW - Macrophages

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Monocytes

KW - Neutrophils

KW - Nitric Oxide

KW - Nitric Oxide Synthase Type II

KW - Tumor Necrosis Factor-alpha

KW - omega-N-Methylarginine

U2 - 10.1371/journal.ppat.1003096

DO - 10.1371/journal.ppat.1003096

M3 - SCORING: Journal article

C2 - 23300453

VL - 9

SP - e1003096

JO - PLOS PATHOG

JF - PLOS PATHOG

SN - 1553-7366

IS - 1

ER -