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IL-22 mediates goblet cell hyperplasia and worm expulsion in intestinal helminth infection

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IL-22 mediates goblet cell hyperplasia and worm expulsion in intestinal helminth infection. / Turner, Jan Eric; Stockinger, Brigitta; Helmby, Helena.

in: PLOS PATHOG, Jahrgang 9, Nr. 10, 01.01.2013, S. e1003698.

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

Harvard

Turner, JE, Stockinger, B & Helmby, H 2013, 'IL-22 mediates goblet cell hyperplasia and worm expulsion in intestinal helminth infection', PLOS PATHOG, Jg. 9, Nr. 10, S. e1003698. https://doi.org/10.1371/journal.ppat.1003698

APA

Turner, J. E., Stockinger, B., & Helmby, H. (2013). IL-22 mediates goblet cell hyperplasia and worm expulsion in intestinal helminth infection. PLOS PATHOG, 9(10), e1003698. https://doi.org/10.1371/journal.ppat.1003698

Vancouver

Turner JE, Stockinger B, Helmby H. IL-22 mediates goblet cell hyperplasia and worm expulsion in intestinal helminth infection. PLOS PATHOG. 2013 Jan 1;9(10):e1003698. https://doi.org/10.1371/journal.ppat.1003698

Bibtex

@article{6f81686911404796bfb960e8f122b1ab,
title = "IL-22 mediates goblet cell hyperplasia and worm expulsion in intestinal helminth infection",
abstract = "Type 2 immune responses are essential in protection against intestinal helminth infections. In this study we show that IL-22, a cytokine important in defence against bacterial infections in the intestinal tract, is also a critical mediator of anti-helminth immunity. After infection with Nippostrongylus brasiliensis, a rodent hookworm, IL-22-deficient mice showed impaired worm expulsion despite normal levels of type 2 cytokine production. The impaired worm expulsion correlated with reduced goblet cell hyperplasia and reduced expression of goblet cell markers. We further confirmed our findings in a second nematode model, the murine whipworm Trichuris muris. T.muris infected IL-22-deficient mice had a similar phenotype to that seen in N.brasiliensis infection, with impaired worm expulsion and reduced goblet cell hyperplasia. Ex vivo and in vitro analysis demonstrated that IL-22 is able to directly induce the expression of several goblet cell markers, including mucins. Taken together, our findings reveal that IL-22 plays an important role in goblet cell activation, and thus, a key role in anti-helminth immunity.",
keywords = "Animals, Gene Expression Regulation, Goblet Cells, Hyperplasia, Immunity, Mucosal, Interleukins, Intestinal Diseases, Parasitic, Mice, Mice, Knockout, Nippostrongylus, Strongylida Infections, Trichuriasis, Trichuris",
author = "Turner, {Jan Eric} and Brigitta Stockinger and Helena Helmby",
year = "2013",
month = jan,
day = "1",
doi = "10.1371/journal.ppat.1003698",
language = "English",
volume = "9",
pages = "e1003698",
journal = "PLOS PATHOG",
issn = "1553-7366",
publisher = "Public Library of Science",
number = "10",

}

RIS

TY - JOUR

T1 - IL-22 mediates goblet cell hyperplasia and worm expulsion in intestinal helminth infection

AU - Turner, Jan Eric

AU - Stockinger, Brigitta

AU - Helmby, Helena

PY - 2013/1/1

Y1 - 2013/1/1

N2 - Type 2 immune responses are essential in protection against intestinal helminth infections. In this study we show that IL-22, a cytokine important in defence against bacterial infections in the intestinal tract, is also a critical mediator of anti-helminth immunity. After infection with Nippostrongylus brasiliensis, a rodent hookworm, IL-22-deficient mice showed impaired worm expulsion despite normal levels of type 2 cytokine production. The impaired worm expulsion correlated with reduced goblet cell hyperplasia and reduced expression of goblet cell markers. We further confirmed our findings in a second nematode model, the murine whipworm Trichuris muris. T.muris infected IL-22-deficient mice had a similar phenotype to that seen in N.brasiliensis infection, with impaired worm expulsion and reduced goblet cell hyperplasia. Ex vivo and in vitro analysis demonstrated that IL-22 is able to directly induce the expression of several goblet cell markers, including mucins. Taken together, our findings reveal that IL-22 plays an important role in goblet cell activation, and thus, a key role in anti-helminth immunity.

AB - Type 2 immune responses are essential in protection against intestinal helminth infections. In this study we show that IL-22, a cytokine important in defence against bacterial infections in the intestinal tract, is also a critical mediator of anti-helminth immunity. After infection with Nippostrongylus brasiliensis, a rodent hookworm, IL-22-deficient mice showed impaired worm expulsion despite normal levels of type 2 cytokine production. The impaired worm expulsion correlated with reduced goblet cell hyperplasia and reduced expression of goblet cell markers. We further confirmed our findings in a second nematode model, the murine whipworm Trichuris muris. T.muris infected IL-22-deficient mice had a similar phenotype to that seen in N.brasiliensis infection, with impaired worm expulsion and reduced goblet cell hyperplasia. Ex vivo and in vitro analysis demonstrated that IL-22 is able to directly induce the expression of several goblet cell markers, including mucins. Taken together, our findings reveal that IL-22 plays an important role in goblet cell activation, and thus, a key role in anti-helminth immunity.

KW - Animals

KW - Gene Expression Regulation

KW - Goblet Cells

KW - Hyperplasia

KW - Immunity, Mucosal

KW - Interleukins

KW - Intestinal Diseases, Parasitic

KW - Mice

KW - Mice, Knockout

KW - Nippostrongylus

KW - Strongylida Infections

KW - Trichuriasis

KW - Trichuris

U2 - 10.1371/journal.ppat.1003698

DO - 10.1371/journal.ppat.1003698

M3 - SCORING: Journal article

C2 - 24130494

VL - 9

SP - e1003698

JO - PLOS PATHOG

JF - PLOS PATHOG

SN - 1553-7366

IS - 10

ER -