Abstract
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.
Highlights
Allergic asthma is an airway chronic inflammatory disease characterized by increased allergen specific IgE production, predominant eosinophilic airway inflammation, increased mucus secretion and development of in vivo hyperreactivity dependent on increased production of Th2 cytokines [1]
Data from human studies showed that CD25hiFoxP3+ T-cell numbers and function were reduced in bronchoalveolar lavage samples from children with asthma compared with those seen in control subjects [17], and that FoxP3 expression by circulating CD4+CD25hi T cells was reduced in asthmatic patients [18]
Immune regulation may ameliorate exaggerated Th1 responses against the infectious agents. With these latter in mind and to explore the cellular mechanisms involved in T. gondii induced protection against allergy we first evaluated if T. gondii infection could modulate allergen-specific T cell proliferation in BALB/c mice
Summary
Allergic asthma is an airway chronic inflammatory disease characterized by increased allergen specific IgE production, predominant eosinophilic airway inflammation, increased mucus secretion and development of in vivo hyperreactivity dependent on increased production of Th2 cytokines [1]. The phenotype expression is dependent upon the interaction between multiple factors including genetic susceptibility, infections and environmental exposures. These two last ones are the major responsible for the observed increased prevalence and morbidity of atopic disorders over the past few decades, especially in developed and developing countries [2,3]. In murine models of allergic airway inflammation many infections or products from the infectious microorganisms protect from the development of allergy by inducing the production of regulatory cytokines such as IL-10 and TGF-b [11,19,20,21,22]. Navarro et al recently showed that oral treatment with bacterial extracts could prevent allergic airway disease in mice through IL-10-dependent and MyD88-dependent mechanisms and conversion of FoxP3- T cells into FoxP3+ regulatory T cells [25]
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