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IL-23 prevents IL-13-dependent tissue repair associated with Ly6C(lo) monocytes in Entamoeba histolytica-induced liver damage

Standard

IL-23 prevents IL-13-dependent tissue repair associated with Ly6C(lo) monocytes in Entamoeba histolytica-induced liver damage. / Noll, Jill; Helk, Elena; Fehling, Helena; Bernin, Hannah; Marggraff, Claudia; Jacobs, Thomas; Huber, Samuel; Pelczar, Penelope; Ernst, Thomas; Ittrich, Harald; Otto, Benjamin; Mittrücker, Hans-Willi; Hölscher, Christoph; Tacke, Frank; Bruchhaus, Iris; Tannich, Egbert; Lotter, Hannelore.

in: J HEPATOL, Jahrgang 64, Nr. 5, 05.2016, S. 1147-57.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Noll, J, Helk, E, Fehling, H, Bernin, H, Marggraff, C, Jacobs, T, Huber, S, Pelczar, P, Ernst, T, Ittrich, H, Otto, B, Mittrücker, H-W, Hölscher, C, Tacke, F, Bruchhaus, I, Tannich, E & Lotter, H 2016, 'IL-23 prevents IL-13-dependent tissue repair associated with Ly6C(lo) monocytes in Entamoeba histolytica-induced liver damage', J HEPATOL, Jg. 64, Nr. 5, S. 1147-57. https://doi.org/10.1016/j.jhep.2016.01.013

APA

Noll, J., Helk, E., Fehling, H., Bernin, H., Marggraff, C., Jacobs, T., Huber, S., Pelczar, P., Ernst, T., Ittrich, H., Otto, B., Mittrücker, H-W., Hölscher, C., Tacke, F., Bruchhaus, I., Tannich, E., & Lotter, H. (2016). IL-23 prevents IL-13-dependent tissue repair associated with Ly6C(lo) monocytes in Entamoeba histolytica-induced liver damage. J HEPATOL, 64(5), 1147-57. https://doi.org/10.1016/j.jhep.2016.01.013

Vancouver

Noll J, Helk E, Fehling H, Bernin H, Marggraff C, Jacobs T et al. IL-23 prevents IL-13-dependent tissue repair associated with Ly6C(lo) monocytes in Entamoeba histolytica-induced liver damage. J HEPATOL. 2016 Mai;64(5):1147-57. https://doi.org/10.1016/j.jhep.2016.01.013

Bibtex

@article{089c1a8450f34355a0d0bc05b5a4e880,
title = "IL-23 prevents IL-13-dependent tissue repair associated with Ly6C(lo) monocytes in Entamoeba histolytica-induced liver damage",
abstract = "BACKGROUND & AIMS: The IL-23/IL-17 axis plays an important role in the pathogenesis of autoimmune diseases and the pathological consequences of infection. We previously showed that immunopathologic mechanisms mediated by inflammatory monocytes underlie the severe focal liver damage induced by the protozoan parasite, Entamoeba histolytica. Here, we analyze the contribution of the IL-23/IL-17 axis to the induction and subsequent recovery from parasite-induced liver damage.METHODS: IL-23p19(-/-), IL-17A/F(-/-), CCR2(-/-), and wild-type (WT) mice were intra-hepatically infected with E. histolytica trophozoites and disease onset and recovery were analyzed by magnetic resonance imaging. Liver-specific gene and protein expression during infection was examined by qPCR, microarray, FACS analysis and immunohistochemistry. Immuno-depletion and substitution experiments were performed in IL-23p19(-/-) and WT mice to investigate the role of IL-13 in disease outcome.RESULTS: Liver damage in infected IL-23p19(-/-), IL-17A/F(-/-), and CCR2(-/-) mice was strongly attenuated compared with that in WT mice. IL-23p19(-/-) mice showed reduced accumulation of IL-17 and CCL2 mRNA and proteins. Increased numbers of IL-13-producing CD11b(+)Ly6C(lo) monocytes were associated with disease attenuation in IL-23p19(-/-) mice. Immuno-depletion of IL-13 in IL-23p19(-/-) mice reversed this attenuation and treatment of infected WT mice with an IL-13/anti-IL-13-mAb complex supported liver recovery.CONCLUSIONS: The IL-23/IL-17 axis plays a critical role in the immunopathology of hepatic amebiasis. IL-13 secreted by CD11b(+)Ly6C(lo) monocytes may be associated with recovery from liver damage. An IL-13/anti-IL13-mAb complex mimics this function, suggesting a novel therapeutic option to support tissue healing after liver damage.",
keywords = "Journal Article, Research Support, Non-U.S. Gov't",
author = "Jill Noll and Elena Helk and Helena Fehling and Hannah Bernin and Claudia Marggraff and Thomas Jacobs and Samuel Huber and Penelope Pelczar and Thomas Ernst and Harald Ittrich and Benjamin Otto and Hans-Willi Mittr{\"u}cker and Christoph H{\"o}lscher and Frank Tacke and Iris Bruchhaus and Egbert Tannich and Hannelore Lotter",
note = "Copyright {\textcopyright} 2016 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.",
year = "2016",
month = may,
doi = "10.1016/j.jhep.2016.01.013",
language = "English",
volume = "64",
pages = "1147--57",
journal = "J HEPATOL",
issn = "0168-8278",
publisher = "Elsevier",
number = "5",

}

RIS

TY - JOUR

T1 - IL-23 prevents IL-13-dependent tissue repair associated with Ly6C(lo) monocytes in Entamoeba histolytica-induced liver damage

AU - Noll, Jill

AU - Helk, Elena

AU - Fehling, Helena

AU - Bernin, Hannah

AU - Marggraff, Claudia

AU - Jacobs, Thomas

AU - Huber, Samuel

AU - Pelczar, Penelope

AU - Ernst, Thomas

AU - Ittrich, Harald

AU - Otto, Benjamin

AU - Mittrücker, Hans-Willi

AU - Hölscher, Christoph

AU - Tacke, Frank

AU - Bruchhaus, Iris

AU - Tannich, Egbert

AU - Lotter, Hannelore

N1 - Copyright © 2016 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

PY - 2016/5

Y1 - 2016/5

N2 - BACKGROUND & AIMS: The IL-23/IL-17 axis plays an important role in the pathogenesis of autoimmune diseases and the pathological consequences of infection. We previously showed that immunopathologic mechanisms mediated by inflammatory monocytes underlie the severe focal liver damage induced by the protozoan parasite, Entamoeba histolytica. Here, we analyze the contribution of the IL-23/IL-17 axis to the induction and subsequent recovery from parasite-induced liver damage.METHODS: IL-23p19(-/-), IL-17A/F(-/-), CCR2(-/-), and wild-type (WT) mice were intra-hepatically infected with E. histolytica trophozoites and disease onset and recovery were analyzed by magnetic resonance imaging. Liver-specific gene and protein expression during infection was examined by qPCR, microarray, FACS analysis and immunohistochemistry. Immuno-depletion and substitution experiments were performed in IL-23p19(-/-) and WT mice to investigate the role of IL-13 in disease outcome.RESULTS: Liver damage in infected IL-23p19(-/-), IL-17A/F(-/-), and CCR2(-/-) mice was strongly attenuated compared with that in WT mice. IL-23p19(-/-) mice showed reduced accumulation of IL-17 and CCL2 mRNA and proteins. Increased numbers of IL-13-producing CD11b(+)Ly6C(lo) monocytes were associated with disease attenuation in IL-23p19(-/-) mice. Immuno-depletion of IL-13 in IL-23p19(-/-) mice reversed this attenuation and treatment of infected WT mice with an IL-13/anti-IL-13-mAb complex supported liver recovery.CONCLUSIONS: The IL-23/IL-17 axis plays a critical role in the immunopathology of hepatic amebiasis. IL-13 secreted by CD11b(+)Ly6C(lo) monocytes may be associated with recovery from liver damage. An IL-13/anti-IL13-mAb complex mimics this function, suggesting a novel therapeutic option to support tissue healing after liver damage.

AB - BACKGROUND & AIMS: The IL-23/IL-17 axis plays an important role in the pathogenesis of autoimmune diseases and the pathological consequences of infection. We previously showed that immunopathologic mechanisms mediated by inflammatory monocytes underlie the severe focal liver damage induced by the protozoan parasite, Entamoeba histolytica. Here, we analyze the contribution of the IL-23/IL-17 axis to the induction and subsequent recovery from parasite-induced liver damage.METHODS: IL-23p19(-/-), IL-17A/F(-/-), CCR2(-/-), and wild-type (WT) mice were intra-hepatically infected with E. histolytica trophozoites and disease onset and recovery were analyzed by magnetic resonance imaging. Liver-specific gene and protein expression during infection was examined by qPCR, microarray, FACS analysis and immunohistochemistry. Immuno-depletion and substitution experiments were performed in IL-23p19(-/-) and WT mice to investigate the role of IL-13 in disease outcome.RESULTS: Liver damage in infected IL-23p19(-/-), IL-17A/F(-/-), and CCR2(-/-) mice was strongly attenuated compared with that in WT mice. IL-23p19(-/-) mice showed reduced accumulation of IL-17 and CCL2 mRNA and proteins. Increased numbers of IL-13-producing CD11b(+)Ly6C(lo) monocytes were associated with disease attenuation in IL-23p19(-/-) mice. Immuno-depletion of IL-13 in IL-23p19(-/-) mice reversed this attenuation and treatment of infected WT mice with an IL-13/anti-IL-13-mAb complex supported liver recovery.CONCLUSIONS: The IL-23/IL-17 axis plays a critical role in the immunopathology of hepatic amebiasis. IL-13 secreted by CD11b(+)Ly6C(lo) monocytes may be associated with recovery from liver damage. An IL-13/anti-IL13-mAb complex mimics this function, suggesting a novel therapeutic option to support tissue healing after liver damage.

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1016/j.jhep.2016.01.013

DO - 10.1016/j.jhep.2016.01.013

M3 - SCORING: Journal article

C2 - 26809113

VL - 64

SP - 1147

EP - 1157

JO - J HEPATOL

JF - J HEPATOL

SN - 0168-8278

IS - 5

ER -