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  4. Inhibition of allergen-induced airway inflammation and hyperreactivity by recombinant lactic-acid bacteria
 
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Inhibition of allergen-induced airway inflammation and hyperreactivity by recombinant lactic-acid bacteria

Resource
Vaccine 24 (33-34): 5931-5936
Journal
Vaccine
Journal Volume
24
Journal Issue
33-34
Pages
5931-5936
Date Issued
2006
Author(s)
YUH-CHYANG CHARNG  
Lin, C.-C.
Hsu, C.-H.
DOI
10.1016/j.vaccine.2005.07.107
URI
http://www.scopus.com/inward/record.url?eid=2-s2.0-33746224290&partnerID=MN8TOARS
http://scholars.lib.ntu.edu.tw/handle/123456789/321869
Abstract
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. ? 2006.
Subjects
Airway hyperreactivity; Allergy; Immunotherapy; Lactic-acid bacteria
SDGs

[SDGs]SDG3

Other Subjects
allergen; immunoglobulin E; immunoglobulin G; placebo; plasmid vector; recombinant lactic acid bacterium vaccine; recombinant vaccine; unclassified drug; airway constriction; allergic asthma; animal cell; animal experiment; animal model; article; bronchus hyperreactivity; comparative study; controlled study; Dermatophagoides pteronyssinus; drug inhibition; eosinophil; female; foraging; immune response; immunoglobulin blood level; immunoglobulin production; lactic acid bacterium; low drug dose; lung lavage; mouse; neutrophil chemotaxis; nonhuman; priority journal; provocation test; sensitization; treatment response; Administration, Oral; Animals; Antigens, Dermatophagoides; Bronchial Hyperreactivity; Bronchoalveolar Lavage Fluid; Desensitization, Immunologic; Enzyme-Linked Immunosorbent Assay; Female; Immunoglobulin E; Immunoglobulin G; Lactobacillus acidophilus; Mice; Probiotics; Respiratory Hypersensitivity
Type
journal article

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