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

• Published in: PloS one 2012-08, Vol.7 (8), p.e43420-e43420
• Main Authors: Fenoy, Ignacio M, Chiurazzi, Romina, Sánchez, Vanesa R, Argenziano, Mariana A, Soto, Ariadna, Picchio, Mariano S, Martin, Valentina, Goldman, Alejandra
• Format: Article
• Language: English
• Subjects: Allergens; Allergic diseases; Allergies; Animals; Antigens; Asthma; Asthma - metabolism; Biology; Bronchoalveolar Lavage; CD4 antigen; CD4 Antigens - biosynthesis; Cell activation; Cell proliferation; Chronic infection; Cytokines; Development and progression; Eosinophils; Epidemiology; Food allergies; Food hypersensitivity; Forkhead Transcription Factors - metabolism; Foxp3 protein; Genetic aspects; Health aspects; Hypersensitivity - metabolism; Immune response; Immune system; Immunoregulation; Infections; Infiltration; Inflammation; Inflammation - pathology; Inflammatory diseases; Interferon; Interferon-gamma - metabolism; Leukocytes (eosinophilic); Lungs; Lymph nodes; Lymph Nodes - pathology; Lymphocytes; Lymphocytes T; Malaria; Mast cells; Mice; Mice, Inbred BALB C; Mice, Inbred C3H; Mice, Knockout; Parasites; Parasitology; Pathogens; Phenotypes; Physiological aspects; Prevention; Reduction; Respiratory Hypersensitivity; Respiratory tract diseases; Studies; T cells; Th2 Cells - cytology; Th2 Cells - parasitology; Thorax; Toxoplasma; Toxoplasma - metabolism; Toxoplasma gondii; Toxoplasmosis - immunology; Toxoplasmosis - physiopathology; Transforming Growth Factor beta - metabolism; γ-Interferon
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0043420

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.