Th2-dependent STAT6-regulated genes in intestinal epithelial cells mediate larval trapping during secondary Heligmosomoides polygyrus bakeri infection.

Bibliographic Details
Title:	Th2-dependent STAT6-regulated genes in intestinal epithelial cells mediate larval trapping during secondary Heligmosomoides polygyrus bakeri infection.
Authors:	Stefanie Westermann, Christoph Schubart, Axel Dietschmann, Kirstin Castiglione, Daniel Radtke, David Voehringer
Source:	PLoS Pathogens, Vol 19, Iss 4, p e1011296 (2023)
Publisher Information:	Public Library of Science (PLoS), 2023.
Publication Year:	2023
Collection:	LCC:Immunologic diseases. Allergy LCC:Biology (General)
Subject Terms:	Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
More Details:	Gastrointestinal helminths are a major health threat worldwide. Alternatively activated macrophages (AAMs) have been shown to contribute to host protection during secondary helminth infections. AAMs express effector molecules that depend on activation of the IL-4- or IL-13-induced transcription factor signal transducer and activator of transcription 6 (STAT6). However, the specific role of STAT6-regulated genes like Arginase-1 (Arg1) from AAMs or STAT6-regulated genes in other cell types for host protection remains unclear. To address this point, we generated mice expressing STAT6 only in macrophages (Mac-STAT6 mouse). In the model of Heligmosomoides polygyrus bakeri (Hpb) infection, Mac-STAT6 mice could not trap larvae in the submucosa of the small intestine after secondary infection. Further, mice lacking Arg1 in hematopoietic and endothelial cells were still protected from secondary Hpb infection. On the other hand, specific deletion of IL-4/IL-13 in T cells blunted AAM polarization, activation of intestinal epithelial cells (IECs) and protective immunity. Deletion of IL-4Rα on IEC also caused loss of larval trapping while AAM polarization remained intact. These results show that Th2-dependent and STAT6-regulated genes in IECs are required and AAMs are not sufficient for protection against secondary Hpb infection by mechanisms that remain to be investigated.
Document Type:	article
File Description:	electronic resource
Language:	English
ISSN:	1553-7366 1553-7374
Relation:	https://doaj.org/toc/1553-7366; https://doaj.org/toc/1553-7374
DOI:	10.1371/journal.ppat.1011296
Access URL:	https://doaj.org/article/3b4c9a548be54e7a81c549bf420874b9
Accession Number:	edsdoj.3b4c9a548be54e7a81c549bf420874b9
Database:	Directory of Open Access Journals
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More Details
ISSN:	15537366 15537374
DOI:	10.1371/journal.ppat.1011296
Published in:	PLoS Pathogens
Language:	English