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International Immunopharmacology 2013-Apr

Induced apoptosis of Th2 lymphocytes and inhibition of airway hyperresponsiveness and inflammation by combined lactic acid bacteria treatment.

Només els usuaris registrats poden traduir articles
Inicieu sessió / registreu-vos
L'enllaç es desa al porta-retalls
Wen-Hsin Lin
Chi-Rei Wu
Hong-Zin Lee
Yueh-Hsiung Kuo
Hung-Shin Wen
Tze-Yi Lin
Chia-Ying Lee
Shi-Ying Huang
Ching-Yuang Lin

Paraules clau

Resum

Several lactic acid bacteria (LAB) demonstrably regulate the immune system and inhibit allergic disease. This study examined whether oral feeding of either Lactobacillus paracasei (L. paracasei) BB5 and/or Lactobacillus rhamnosus (L. rhamnosus) BB1 suppresses ovalbumin (OVA)-induced airway hyperresponsiveness (AHR) and inflammation in a murine model. OVA-specific immune responses, cell profile of bronchoalveolar lavage fluid (BALF), and airway AHR were assessed following OVA and methacholine challenge. We investigated whether LAB can enhance CD4(+)FoxP3(+) and CD8(+)FoxP3(+) regulatory T (Treg) cells in splenic cells and apoptosis of CD4(+)IL-4(+) T cells. Results found oral administration of combined LAB better than single L. paracasei or L. rhamnosus strain, improving Penh ratio after challenge with methacholine. High-dose combined LAB starkly decreased synthesis of OVA-specific IgE and IgG2a levels, as well as eosinophils infiltration in BALF. In addition, CD4(+)IL-4(+) T cells decreased while CD4(+)FoxP3(+) and CD8(+)FoxP3(+) Treg cells increased significantly in splenic mononuclear cells of high-dose combined LAB group. Findings indicate allergen-induced AHR and airway allergic inflammation suppressed by enhances CD4(+)FoxP3(+) and CD8(+)FoxP3(+) Treg populations as well as Th1 cell response after treating with combined LAB. This study may provide a basis for developing a novel therapeutic or protective method for airway allergic disease.

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