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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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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
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author Lee, Young-Sil
Park, Gun-Seok
Ko, Seung-Hyun
Yang, Won-Kyung
Seo, Hye-Jin
Kim, Seung-Hyung
Jeong, Nara
Kang, Jihee
author_facet Lee, Young-Sil
Park, Gun-Seok
Ko, Seung-Hyun
Yang, Won-Kyung
Seo, Hye-Jin
Kim, Seung-Hyung
Jeong, Nara
Kang, Jihee
author_sort Lee, Young-Sil
collection PubMed
description 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.
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spelling pubmed-101742542023-05-12 Lactobacillus paracasei ATG-E1 improves particulate matter 10 plus diesel exhaust particles (PM(10)D)-induced airway inflammation by regulating immune responses Lee, Young-Sil Park, Gun-Seok Ko, Seung-Hyun Yang, Won-Kyung Seo, Hye-Jin Kim, Seung-Hyung Jeong, Nara Kang, Jihee Front Microbiol Microbiology 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. Frontiers Media S.A. 2023-04-27 /pmc/articles/PMC10174254/ /pubmed/37180255 http://dx.doi.org/10.3389/fmicb.2023.1145546 Text en Copyright © 2023 Lee, Park, Ko, Yang, Seo, Kim, Jeong and Kang. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Lee, Young-Sil
Park, Gun-Seok
Ko, Seung-Hyun
Yang, Won-Kyung
Seo, Hye-Jin
Kim, Seung-Hyung
Jeong, Nara
Kang, Jihee
Lactobacillus paracasei ATG-E1 improves particulate matter 10 plus diesel exhaust particles (PM(10)D)-induced airway inflammation by regulating immune responses
title Lactobacillus paracasei ATG-E1 improves particulate matter 10 plus diesel exhaust particles (PM(10)D)-induced airway inflammation by regulating immune responses
title_full Lactobacillus paracasei ATG-E1 improves particulate matter 10 plus diesel exhaust particles (PM(10)D)-induced airway inflammation by regulating immune responses
title_fullStr Lactobacillus paracasei ATG-E1 improves particulate matter 10 plus diesel exhaust particles (PM(10)D)-induced airway inflammation by regulating immune responses
title_full_unstemmed Lactobacillus paracasei ATG-E1 improves particulate matter 10 plus diesel exhaust particles (PM(10)D)-induced airway inflammation by regulating immune responses
title_short Lactobacillus paracasei ATG-E1 improves particulate matter 10 plus diesel exhaust particles (PM(10)D)-induced airway inflammation by regulating immune responses
title_sort lactobacillus paracasei atg-e1 improves particulate matter 10 plus diesel exhaust particles (pm(10)d)-induced airway inflammation by regulating immune responses
topic Microbiology
url 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
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