한빛사 논문
Yu-Jin Jeonga,1, Chang-Ung Kimc,1, Kyung-Soo Leea,b, Ji Hyung Kimd, Seo Young Parka, Ahn Young Jeongb,c, Jun Bong Leee, Doo-Jin Kimb,c, Young-Jun Parka,b, Moo-Seung Leea,b
aEnvironmental Diseases Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB), 125 Gwahak-ro, Daejeon, 34141, Republic of Korea
bDepartment of Biomolecular Science, KRIBB School of Bioscience, Korea University of Science and Technology (UST), 127 Gajeong-ro, Yuseong-gu, Daejeon, 34113, Republic of Korea
cInfectious Disease Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB), 125 Gwahak-ro, Daejeon, 34141, Republic of Korea
dDepartment of Food Science and Biotechnology, Gachon University, Seongnam, 13120, Republic of Korea
eCollege of Veterinary Medicine & Institute of Veterinary Science, Kangwon National University, Chuncheon, Kangwon, 24341, Republic of Korea
1These authors contributed equally to this work.
Corresponding author: Moo-Seung Lee
Abstract
Atmospheric particulate matter (PM) contains a mixture of chemical and biological elements that pose threat to human health by increasing susceptibility to respiratory diseases. Although the identification of the microorganisms composing the PM has been assessed, their immunological impacts are still questionable. Here, we examined the mechanisms responsible for the pathogenicity of Pseudomonas stutzeri PM101005 (PMPS), a bacterium isolated from fine dust, in lung epithelial cells, alveolar cells, and macrophages. Relative to its comparative strain Pseudomonas stutzeri (PS), infections with PMPS induced higher production of inflammatory cytokines and chemokines, mediated by the activation of NF-κB and MAPK signaling pathways. Additionally, with three-dimensional (3D) airway spheroids which mimic the human bronchial epithelium, we confirmed that PMPS infections lead to relatively higher induction of pro-inflammatory cytokines than PM infections. Consistent results were observed in murine models as the infections with PMPS provoked greater inflammatory responses than the infections with PS. These PMPS-induced responses were mediated by the signaling pathways of the Toll-like receptors (TLRs), which regulated PMPS infection and played an important role in the expression of the antibiotic peptide β-defensin 3 (BD3) that suppressed PMPS proliferation. Moreover, PM pretreatment enhanced inflammatory responses and tissue damage of PMPS, while reducing BD3 expression. Overall, these results indicate that PM-isolated PMPS induce TLR-mediated inflammatory responses in lung tissues, and contributes to the understanding of the etiology of PM-induced respiratory damage.
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