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Pseudomonas aeruginosa Induced Lung Injury Model
Published on: October 29, 2014
Pseudomonas stutzeri PM101005 inhaled with atmospheric particulate matter induces lung damage through inflammatory
Yu-Jin Jeong1, Chang-Ung Kim2, Kyung-Soo Lee3
1Environmental Diseases Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB), 125 Gwahak-ro, Daejeon, 34141, Republic of Korea.
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.
Insights
Particulate matter-associated bacteria like Pseudomonas stutzeri PM101005 (PMPS) trigger significant inflammatory responses in lung tissues. These responses, mediated by Toll-like receptors (TLRs), contribute to respiratory damage and highlight the immunological impact of airborne microbes.
Area of Science:
- Environmental microbiology
- Immunology
- Respiratory medicine
Background:
- Atmospheric particulate matter (PM) poses respiratory health risks due to its complex composition.
- The immunological effects of microorganisms within PM are not fully understood.
- Pseudomonas stutzeri PM101005 (PMPS) is a bacterium isolated from fine dust with potential pathogenic mechanisms.
Purpose of the Study:
- To investigate the pathogenicity of PMPS in lung epithelial cells, alveolar cells, and macrophages.
- To elucidate the immunological mechanisms underlying PMPS-induced inflammation.
- To compare the inflammatory potential of PMPS with its non-PM-associated strain (PS) and PM itself.
Main Methods:
- In vitro studies using lung epithelial cells, alveolar cells, and macrophages.
- Three-dimensional (3D) airway spheroid models to mimic human bronchial epithelium.
- Murine models to assess in vivo inflammatory responses.
- Analysis of NF-κB, MAPK, and Toll-like receptor (TLR) signaling pathways.
- Measurement of cytokine, chemokine, and β-defensin 3 (BD3) expression.
Main Results:
- PMPS infection induced higher levels of inflammatory cytokines and chemokines than PS infection, mediated by NF-κB and MAPK pathways.
- PMPS triggered greater pro-inflammatory cytokine induction in 3D airway spheroids compared to PM alone.
- Murine models showed enhanced inflammatory responses and tissue damage with PMPS compared to PS.
- TLR signaling pathways mediated PMPS infection and regulated BD3 expression, which suppressed bacterial proliferation.
- PM pretreatment exacerbated inflammatory responses and tissue damage while reducing BD3 expression.
Conclusions:
- PM-isolated PMPS induces significant TLR-mediated inflammatory responses in lung tissues.
- PMPS contributes to the understanding of the etiology of PM-induced respiratory damage.
- The interaction between PM, bacteria, and host immune responses is crucial for respiratory health.
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