Low-Dose Intestinal Trichuris muris Infection Alters the Lung Immune Microenvironment and Can Suppress Allergic Airway Inflammation

Low-Dose Intestinal Trichuris muris Infection Alters the Lung Immune Microenvironment and Can Suppress Allergic Airway Inflammation

Immunological cross talk between mucosal tissues such as the intestine and the lung is poorly defined during homeostasis and disease. Here, we show that a low-dose infection with the intestinally restricted helminth parasite Trichuris muris results in the production of Th1 cell-dependent gamma inter...

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Main Authors: Chenery, Alistair L., Antignano, Frann, Burrows, Kyle, Scheer, Sebastian, Perona-Wright, Georgia, Zaph, Colby
Format: Online
Language:English
Published: American Society for Microbiology 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4730564/
id pubmed-4730564
recordtype oai_dc
spelling pubmed-47305642016-02-13 Low-Dose Intestinal Trichuris muris Infection Alters the Lung Immune Microenvironment and Can Suppress Allergic Airway Inflammation Chenery, Alistair L. Antignano, Frann Burrows, Kyle Scheer, Sebastian Perona-Wright, Georgia Zaph, Colby Fungal and Parasitic Infections Immunological cross talk between mucosal tissues such as the intestine and the lung is poorly defined during homeostasis and disease. Here, we show that a low-dose infection with the intestinally restricted helminth parasite Trichuris muris results in the production of Th1 cell-dependent gamma interferon (IFN-γ) and myeloid cell-derived interleukin-10 (IL-10) in the lung without causing overt airway pathology. This cross-mucosal immune response in the lung inhibits the development of papain-induced allergic airway inflammation, an innate cell-mediated type 2 airway inflammatory disease. Thus, we identify convergent and nonredundant roles of adaptive and innate immunity in mediating cross-mucosal suppression of type 2 airway inflammation during low-dose helminth-induced intestinal inflammation. These results provide further insight in identifying novel intersecting immune pathways elicited by gut-to-lung mucosal cross talk. American Society for Microbiology 2016-01-25 /pmc/articles/PMC4730564/ /pubmed/26644379 http://dx.doi.org/10.1128/IAI.01240-15 Text en Copyright © 2016 Chenery et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license (http://creativecommons.org/licenses/by/4.0/) .
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Chenery, Alistair L.
Antignano, Frann
Burrows, Kyle
Scheer, Sebastian
Perona-Wright, Georgia
Zaph, Colby
spellingShingle Chenery, Alistair L.
Antignano, Frann
Burrows, Kyle
Scheer, Sebastian
Perona-Wright, Georgia
Zaph, Colby
Low-Dose Intestinal Trichuris muris Infection Alters the Lung Immune Microenvironment and Can Suppress Allergic Airway Inflammation
author_facet Chenery, Alistair L.
Antignano, Frann
Burrows, Kyle
Scheer, Sebastian
Perona-Wright, Georgia
Zaph, Colby
author_sort Chenery, Alistair L.
title Low-Dose Intestinal Trichuris muris Infection Alters the Lung Immune Microenvironment and Can Suppress Allergic Airway Inflammation
title_short Low-Dose Intestinal Trichuris muris Infection Alters the Lung Immune Microenvironment and Can Suppress Allergic Airway Inflammation
title_full Low-Dose Intestinal Trichuris muris Infection Alters the Lung Immune Microenvironment and Can Suppress Allergic Airway Inflammation
title_fullStr Low-Dose Intestinal Trichuris muris Infection Alters the Lung Immune Microenvironment and Can Suppress Allergic Airway Inflammation
title_full_unstemmed Low-Dose Intestinal Trichuris muris Infection Alters the Lung Immune Microenvironment and Can Suppress Allergic Airway Inflammation
title_sort low-dose intestinal trichuris muris infection alters the lung immune microenvironment and can suppress allergic airway inflammation
description Immunological cross talk between mucosal tissues such as the intestine and the lung is poorly defined during homeostasis and disease. Here, we show that a low-dose infection with the intestinally restricted helminth parasite Trichuris muris results in the production of Th1 cell-dependent gamma interferon (IFN-γ) and myeloid cell-derived interleukin-10 (IL-10) in the lung without causing overt airway pathology. This cross-mucosal immune response in the lung inhibits the development of papain-induced allergic airway inflammation, an innate cell-mediated type 2 airway inflammatory disease. Thus, we identify convergent and nonredundant roles of adaptive and innate immunity in mediating cross-mucosal suppression of type 2 airway inflammation during low-dose helminth-induced intestinal inflammation. These results provide further insight in identifying novel intersecting immune pathways elicited by gut-to-lung mucosal cross talk.
publisher American Society for Microbiology
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4730564/
_version_ 1613529775913041920

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