Toxoplasma gondii infection induces suppression in a mouse model of allergic airway inflammation.

Allergic asthma is an inflammatory disorder characterized by infiltration of the airway wall with inflammatory cells driven mostly by activation of Th2-lymphocytes, eosinophils and mast cells. There is a link between increased allergy and a reduction of some infections in Western countries. Epidemio...

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Main Authors: Ignacio M Fenoy, Romina Chiurazzi, Vanesa R Sánchez, Mariana A Argenziano, Ariadna Soto, Mariano S Picchio, Valentina Martin, Alejandra Goldman
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS ONE
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22952678/?tool=EBI
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author Ignacio M Fenoy
Romina Chiurazzi
Vanesa R Sánchez
Mariana A Argenziano
Ariadna Soto
Mariano S Picchio
Valentina Martin
Alejandra Goldman
author_facet Ignacio M Fenoy
Romina Chiurazzi
Vanesa R Sánchez
Mariana A Argenziano
Ariadna Soto
Mariano S Picchio
Valentina Martin
Alejandra Goldman
author_sort Ignacio M Fenoy
collection DOAJ
description Allergic asthma is an inflammatory disorder characterized by infiltration of the airway wall with inflammatory cells driven mostly by activation of Th2-lymphocytes, eosinophils and mast cells. There is a link between increased allergy and a reduction of some infections in Western countries. Epidemiological data also show that respiratory allergy is less frequent in people exposed to orofecal and foodborne microbes such as Toxoplasma gondii. We previously showed that both acute and chronic parasite T. gondii infection substantially blocked development of airway inflammation in adult BALB/c mice. Based on the high levels of IFN-γ along with the reduction of Th2 phenotype, we hypothesized that the protective effect might be related to the strong Th1 immune response elicited against the parasite. However, other mechanisms could also be implicated. The possibility that regulatory T cells inhibit allergic diseases has received growing support from both animal and human studies. Here we investigated the cellular mechanisms involved in T. gondii induced protection against allergy. Our results show for the first time that thoracic lymph node cells from mice sensitized during chronic T. gondii infection have suppressor activity. Suppression was detected both in vitro, on allergen specific T cell proliferation and in vivo, on allergic lung inflammation after adoptive transference from infected/sensitized mice to previously sensitized animals. This ability was found to be contact-independent and correlated with high levels of TGF-β and CD4(+)FoxP3(+) cells.
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spelling doaj.art-2f0fe4178fea4b9d968e1c75b45c58f62022-12-21T23:09:51ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0178e4342010.1371/journal.pone.0043420Toxoplasma gondii infection induces suppression in a mouse model of allergic airway inflammation.Ignacio M FenoyRomina ChiurazziVanesa R SánchezMariana A ArgenzianoAriadna SotoMariano S PicchioValentina MartinAlejandra GoldmanAllergic asthma is an inflammatory disorder characterized by infiltration of the airway wall with inflammatory cells driven mostly by activation of Th2-lymphocytes, eosinophils and mast cells. There is a link between increased allergy and a reduction of some infections in Western countries. Epidemiological data also show that respiratory allergy is less frequent in people exposed to orofecal and foodborne microbes such as Toxoplasma gondii. We previously showed that both acute and chronic parasite T. gondii infection substantially blocked development of airway inflammation in adult BALB/c mice. Based on the high levels of IFN-γ along with the reduction of Th2 phenotype, we hypothesized that the protective effect might be related to the strong Th1 immune response elicited against the parasite. However, other mechanisms could also be implicated. The possibility that regulatory T cells inhibit allergic diseases has received growing support from both animal and human studies. Here we investigated the cellular mechanisms involved in T. gondii induced protection against allergy. Our results show for the first time that thoracic lymph node cells from mice sensitized during chronic T. gondii infection have suppressor activity. Suppression was detected both in vitro, on allergen specific T cell proliferation and in vivo, on allergic lung inflammation after adoptive transference from infected/sensitized mice to previously sensitized animals. This ability was found to be contact-independent and correlated with high levels of TGF-β and CD4(+)FoxP3(+) cells.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22952678/?tool=EBI
spellingShingle Ignacio M Fenoy
Romina Chiurazzi
Vanesa R Sánchez
Mariana A Argenziano
Ariadna Soto
Mariano S Picchio
Valentina Martin
Alejandra Goldman
Toxoplasma gondii infection induces suppression in a mouse model of allergic airway inflammation.
PLoS ONE
title Toxoplasma gondii infection induces suppression in a mouse model of allergic airway inflammation.
title_full Toxoplasma gondii infection induces suppression in a mouse model of allergic airway inflammation.
title_fullStr Toxoplasma gondii infection induces suppression in a mouse model of allergic airway inflammation.
title_full_unstemmed Toxoplasma gondii infection induces suppression in a mouse model of allergic airway inflammation.
title_short Toxoplasma gondii infection induces suppression in a mouse model of allergic airway inflammation.
title_sort toxoplasma gondii infection induces suppression in a mouse model of allergic airway inflammation
url https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22952678/?tool=EBI
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