کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2407581 1551792 2006 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Inhibition of allergen-induced airway inflammation and hyperreactivity by recombinant lactic-acid bacteria
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Inhibition of allergen-induced airway inflammation and hyperreactivity by recombinant lactic-acid bacteria
چکیده انگلیسی

Recombinant lactic-acid bacteria (LAB) are able to inhibit allergen-specific T-cell responses. In this study, we examined whether oral feeding of recombinant LAB was able to suppress allergen-induced airway inflammation and hyperreactivity (AHR) in a murine model. Animals were intraperitoneally sensitized with Dermatophagoides pteronyssinus group-5 allergen (Der p 5) and orally treated with recombinant LAB containing a plasmid-encoded Der p 5 gene or placebo on day 7 and day 14 for three days consecutively. Twenty-one days after sensitization, mice underwent inhalational challenging. Der p 5-specific immunological responses including changes to specific immunoglobulin G and E (IgE) levels, the presence of cells in the bronchoalveolar lavage fluid (BALF), and AHR were assessed following this inhalational challenge. We demonstrated that oral feeding of recombinant LAB could significantly decrease the synthesis of Der p 5-specific IgE, and AHR. Furthermore, following such treatment, we also noted that both neutrophils and eosinophils had infiltrated the BALF to a significantly lower extent, when compared to the vehicle-treated group. Neither recombinant allergen nor LAB alone was able to suppress allergen-induced immune responses. Our findings suggest that treatment with recombinant LAB at a low dose can suppress allergen-induced airway allergic inflammation, this providing a basis for developing a novel therapeutic method for allergic airway diseases.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Vaccine - Volume 24, Issues 33–34, 14 August 2006, Pages 5931–5936
نویسندگان
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