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Administration of Lactobacillus paracasei HB89 mitigates PM(2.5)-induced enhancement of inflammation and allergic airway response in murine asthma model

PM(2.5) causes abnormal immune response and asthma in animals. In this study, a Balb/c mouse animal model was exposed to PM(2.5) to induce asthma. Lactobacillus paracasei HB89 was fed at the same time, in order to observe whether L. paracasei HB89 mitigates respiratory tract allergies stimulated by...

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Detalles Bibliográficos
Autores principales: Lin, Ching-Hung, Tseng, Chia-Yi, Chao, Ming-Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7721166/
https://www.ncbi.nlm.nih.gov/pubmed/33284823
http://dx.doi.org/10.1371/journal.pone.0243062
Descripción
Sumario:PM(2.5) causes abnormal immune response and asthma in animals. In this study, a Balb/c mouse animal model was exposed to PM(2.5) to induce asthma. Lactobacillus paracasei HB89 was fed at the same time, in order to observe whether L. paracasei HB89 mitigates respiratory tract allergies stimulated by PM(2.5). The results showed that PM(2.5) stimulated a significant increase in white blood cells and immunoglobulin (IgE) in OVA-induced allergic Balb/c mice, and IgE in the blood further triggered the release of histamine in the lung immune cells. This not only increased overall immune cell counts, but the lymphocyte counts also increased significantly, resulting in significant inhibitions of cytokines INF-r and TGF-β, and induction of IL-4, IL-5, IL-13 and IL-17a. After feeding with HB89, apart from the absence of observable changes in body weight, the total white blood cell count in the animal blood and IgE response were also be reduced; the proliferation of immune cells in the lungs caused by PM(2.5) was slowed down; and histamine and cytokines INF-r and TGF-β were secreted in large quantities, but IL- 4, IL-5, IL-13, IL-17a were inhibited, which effectively reduced the possibility of asthma induction.