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Lactobacillus paracasei ATG-E1 improves particulate matter 10 plus diesel exhaust particles (PM(10)D)-induced airway inflammation by regulating immune responses

Particulate matter (PM) exposure can adversely affect respiratory function. Probiotics can alleviate the inflammatory responses in respiratory diseases. We examined the protective effects of Lactobacillus paracasei ATG-E1 isolated from the feces of a newborn baby against airway inflammation in a PM(...

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Detalles Bibliográficos
Autores principales: Lee, Young-Sil, Park, Gun-Seok, Ko, Seung-Hyun, Yang, Won-Kyung, Seo, Hye-Jin, Kim, Seung-Hyung, Jeong, Nara, Kang, Jihee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10174254/
https://www.ncbi.nlm.nih.gov/pubmed/37180255
http://dx.doi.org/10.3389/fmicb.2023.1145546
Descripción
Sumario:Particulate matter (PM) exposure can adversely affect respiratory function. Probiotics can alleviate the inflammatory responses in respiratory diseases. We examined the protective effects of Lactobacillus paracasei ATG-E1 isolated from the feces of a newborn baby against airway inflammation in a PM(10) plus diesel exhaust particle (DEP) (PM(10)D)-induced airway inflammation model. BALB/c mice were exposed to PM(10)D by intranasal injection three times at 3-day intervals for 12 days, and L. paracasei ATG-E1 was administered orally for 12 days. Analysis of immune cell population and expression of various inflammatory mediators and gut barrier-related genes were determined in bronchoalveolar lavage fluid (BALF), lung, peyer’s patch, and small intestine. A histological analysis of the lungs was performed. In addition, the in vitro safety and their safety in genomic analyses were examined. L. paracasei ATG-E1 was found to be safe in vitro and by genomic analysis. L. paracasei ATG-E1 suppressed neutrophil infiltration and the number of CD4(+), CD4(+)CD69(+), CD62L(–)CD44(+high), CD21/35(+)B220(+), and Gr-1(+)CD11b(+) cells, as well as the expression of inflammatory mediators, including chemokine (C-X-C motif) ligand (CXCL)-1, macrophage inflammatory protein (MIP)-2, interleukin (IL)-17a, tumor necrosis factor (TNF)-α, and IL-6 in BALF and lungs in PM(10)D-induced airway inflammation. It protected against histopathological damage in the lungs of mice with PM(10)D-induced airway inflammation. L. paracasei ATG-E1 concomitantly increased the expression levels of the gut barrier function-related genes occludin, claudin-1, and IL-10 in the small intestine, with an increased number of CD4(+) and CD4(+)CD25(+) immune cells in the peyer’s patch. L. paracasei ATG-E1 suppressed immune activation and airway inflammatory responses in the airways and lungs by restoring the lung damage by PM(10)D. It also regulated intestinal immunity and ameliorated the gut barrier function in the ileum. These results indicate the potential of L. paracasei ATG-E1 as an protective and therapeutic agent against airway inflammation and respiratory diseases.