{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T04:18:31Z","timestamp":1787026711890,"version":"build-2736575974"},"reference-count":44,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2023,4,27]],"date-time":"2023-04-27T00:00:00Z","timestamp":1682553600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Microbiol."],"abstract":"<jats:p>\n                    Particulate matter (PM) exposure can adversely affect respiratory function. Probiotics can alleviate the inflammatory responses in respiratory diseases. We examined the protective effects of\n                    <jats:italic>Lactobacillus paracasei<\/jats:italic>\n                    ATG-E1 isolated from the feces of a newborn baby against airway inflammation in a PM\n                    <jats:sub>10<\/jats:sub>\n                    plus diesel exhaust particle (DEP) (PM\n                    <jats:sub>10<\/jats:sub>\n                    D)-induced airway inflammation model. BALB\/c mice were exposed to PM\n                    <jats:sub>10<\/jats:sub>\n                    D by intranasal injection three times at 3-day intervals for 12 days, and\n                    <jats:italic>L. paracasei<\/jats:italic>\n                    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\u2019s patch, and small intestine. A histological analysis of the lungs was performed. In addition, the\n                    <jats:italic>in vitro<\/jats:italic>\n                    safety and their safety in genomic analyses were examined.\n                    <jats:italic>L. paracasei<\/jats:italic>\n                    ATG-E1 was found to be safe\n                    <jats:italic>in vitro<\/jats:italic>\n                    and by genomic analysis.\n                    <jats:italic>L. paracasei<\/jats:italic>\n                    ATG-E1 suppressed neutrophil infiltration and the number of CD4\n                    <jats:sup>+<\/jats:sup>\n                    , CD4\n                    <jats:sup>+<\/jats:sup>\n                    CD69\n                    <jats:sup>+<\/jats:sup>\n                    , CD62L\n                    <jats:sup>\u2013<\/jats:sup>\n                    CD44\n                    <jats:sup>+high<\/jats:sup>\n                    , CD21\/35\n                    <jats:sup>+<\/jats:sup>\n                    B220\n                    <jats:sup>+<\/jats:sup>\n                    , and Gr-1\n                    <jats:sup>+<\/jats:sup>\n                    CD11b\n                    <jats:sup>+<\/jats:sup>\n                    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)-\u03b1, and IL-6 in BALF and lungs in PM\n                    <jats:sub>10<\/jats:sub>\n                    D-induced airway inflammation. It protected against histopathological damage in the lungs of mice with PM\n                    <jats:sub>10<\/jats:sub>\n                    D-induced airway inflammation.\n                    <jats:italic>L. paracasei<\/jats:italic>\n                    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\n                    <jats:sup>+<\/jats:sup>\n                    and CD4\n                    <jats:sup>+<\/jats:sup>\n                    CD25\n                    <jats:sup>+<\/jats:sup>\n                    immune cells in the peyer\u2019s patch.\n                    <jats:italic>L. paracasei<\/jats:italic>\n                    ATG-E1 suppressed immune activation and airway inflammatory responses in the airways and lungs by restoring the lung damage by PM\n                    <jats:sub>10<\/jats:sub>\n                    D. It also regulated intestinal immunity and ameliorated the gut barrier function in the ileum. These results indicate the potential of\n                    <jats:italic>L. paracasei<\/jats:italic>\n                    ATG-E1 as an protective and therapeutic agent against airway inflammation and respiratory diseases.\n                  <\/jats:p>","DOI":"10.3389\/fmicb.2023.1145546","type":"journal-article","created":{"date-parts":[[2023,4,27]],"date-time":"2023-04-27T00:28:25Z","timestamp":1682555305000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":8,"title":["Lactobacillus paracasei ATG-E1 improves particulate matter 10 plus diesel exhaust particles (PM10D)-induced airway inflammation by regulating immune responses"],"prefix":"10.3389","volume":"14","author":[{"given":"Young-Sil","family":"Lee","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gun-Seok","family":"Park","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seung-Hyun","family":"Ko","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Won-Kyung","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hye-Jin","family":"Seo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seung-Hyung","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nara","family":"Jeong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jihee","family":"Kang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2023,4,27]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"269","DOI":"10.1016\/j.taap.2005.01.023","article-title":"Regulation of cytokine production in human alveolar macrophages and airway epithelial cells in response to ambient air pollution particles: further mechanistic studies.","author":"Becker","year":"2005","journal-title":"Toxicol. 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