Lactobacillus paracasei ATG-E1 improves particulate matter 10 plus diesel exhaust particles (PM10D)-induced airway inflammation by regulating immune responses

Young-Sil Lee; Gun-Seok Park; Seung-Hyun Ko; Won-Kyung Yang; Hye-Jin Seo; Seung-Hyung Kim; Nara Jeong; Jihee Kang

doi:10.3389/fmicb.2023.1145546

Lactobacillus paracasei ATG-E1 improves particulate matter 10 plus diesel exhaust particles (PM₁₀D)-induced airway inflammation by regulating immune responses

Front Microbiol. 2023 Apr 27:14:1145546. doi: 10.3389/fmicb.2023.1145546. eCollection 2023.

Authors

Young-Sil Lee^#¹, Gun-Seok Park^#¹, Seung-Hyun Ko¹, Won-Kyung Yang², Hye-Jin Seo², Seung-Hyung Kim², Nara Jeong¹, Jihee Kang¹

Affiliations

¹ AtoGen Co., Ltd., Daejeon, Republic of Korea.
² Institute of Traditional Medicine and Bioscience, Daejeon University, Daejeon, Republic of Korea.

^# Contributed equally.

Abstract

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 PM₁₀ plus diesel exhaust particle (DEP) (PM₁₀D)-induced airway inflammation model. BALB/c mice were exposed to PM₁₀D 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 PM₁₀D-induced airway inflammation. It protected against histopathological damage in the lungs of mice with PM₁₀D-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 PM₁₀D. 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.

Keywords: Lactobacillus paracasei; airway inflammation; diesel exhaust particles; particulate matter; probiotics.